Given the experience in the treatment of chronic diseases such as cardiovascular disease and diabetes, the concepts of treating to target and tight control have been gradually expanded to other specialties in medicine and other diseases. Among them, treating to target is a treatment concept that allows clinical treatment to have a clear direction and goal, that is, once the disease is diagnosed, it should be induced toward the goal of complete remission, and even if complete remission cannot be achieved, it should be controlled at a low level of activity as much as possible in order to prevent the harm of the disease to the organism, which is called “treating to target This is called “target therapy” [1]. Target therapy is achieved through a “tightly controlled” treatment process. Systemic lupus erythematosus (SLE) is a chronic, incurable disease, and evidence-based follow-up studies have shown that failure to achieve complete remission and sustained disease activity with initial treatment is an indication of poor prognosis in SLE. Therefore, the concept of target therapy needs to be introduced for SLE as well. 1. how to implement target therapy in SLE In rheumatology, target therapy for rheumatoid arthritis (RA) has been gradually recognized and mastered by specialists [1], the concept of target therapy for SLE has not yet been developed [2]. SLE is a highly heterogeneous disease with different mild, severe, acute and slow disease, different physical status of patients and their sensitivity and tolerance to drugs, etc. [3]. Therefore, targeted therapy requires individualization of an initial regimen of induction therapy and, at follow-up, assessment and adjustment of the regimen based on the patient’s response to therapy to ensure progressive improvement of the disease toward the goal of remission or hypoactivity. Because SLE is much more heterogeneous and variable than RA, a “tight control” program for SLE cannot be mechanically defined as a monthly assessment and 3-monthly adjustment of the treatment plan, as is the case for RA. Rather, the timing of assessment and adjustment of treatment is determined on a case-by-case basis. For example, patients with critical lupus need to be evaluated and adjusted at any time; inpatients with severe SLE also need to review clinical and laboratory indicators within a short period of time; patients discharged from the hospital and those initially treated in outpatient clinics usually need to be reviewed and evaluated every 1-2 weeks in the first month, and monthly thereafter; after the disease is controlled at low activity level, review and evaluate every 3 months; after remission, if the disease is asymptomatic, review and evaluate every 3-6 months. If the disease is in remission and there are no symptoms, the assessment can be done every 3~6 months. The target treatment for SLE needs to be based on evidence-based medicine, which organically combines the best clinical research evidence, the clinical experience of physicians and the current situation and needs of patients. The first step requires clinical assessment of individual patients for disease activity, severity and prognosis. Many follow-up studies with evidence-based medical implications in the last decade or so have shown that the indications for poor prognosis in SLE include: pulmonary hypertension, interstitial lung lesions, gastrointestinal vascular lesions, central nervous system damage, and lupus nephritis. In lupus nephritis, pathological changes directly affect the prognosis, and massive proteinuria (>3,5g/24hr) for 3 months, persistent hypertension, and increased blood creatinine at the onset of the disease are also clinical indications of poor prognosis. In the author’s experience, very low complement C3 (e.g., <0, 2 umol/L) is often indicative of a very unstable disease that can suddenly transform into a lupus crisis without any other prognosis and requires clinical vigilance. Randomized controlled trials (RCTs) for SLE therapeutics are only important references and should not be blindly copied in clinical treatment decisions. In addition, the disease and prognosis of SLE are ethnically related, and SLE is more severe in people of color than in Caucasians, so Western RCTs may not be suitable for Chinese patients. The RCT may not be suitable for Chinese patients either. Treatment of SLE requires an individualized initial regimen of induction therapy based on an assessment of the disease. The response to treatment, including efficacy and tolerability, must be closely monitored at the beginning of the initial regimen in order to adjust to the most appropriate drug combination and dose for the patient. For example, in patients with SLE combined with moderate to severe pulmonary hypertension, in addition to symptomatic antihypertensive agents for pulmonary artery pressure and appropriate anticoagulation therapy, it is more important to have a strong induction of remission therapy: standard high-dose hormone (prednisone 1 mg/kg body weight daily) and intensive therapy with cyclophosphamide (intravenous cyclophosphamide 200 mg every other day or 600 mg once a week). For mild to moderate SLE (those with only rash, arthritis, and mild hypocomplementemia), initial therapy may require only: methotrexate 15 mg/wk, prednisone 10 mg/d, and hydroxychloroquine 400 mg/d. During follow-up therapy, the treatment regimen is evaluated and adjusted according to the patient's response to therapy to ensure that the disease improves gradually toward the goal of remission or hypoactivity, and the intensity of drug therapy was gradually reduced with the improvement of the disease. After complete remission, some patients may be able to gradually withdraw hormones or even discontinue medication. However, discontinuation of medication is not the same as cure, and even after discontinuation of medication, review is still required every 3-6 months. If there is a "subclinical relapse", milder drugs may be needed to control it. Hormone is the basic drug for the treatment of SLE, but the role of hormone is mainly anti-inflammatory and relieves the inflammation in the acute stage. Therefore, the dose of hormone depends on the intensity of inflammatory reaction at that time. For example, for SLE combined with hemorrhagic alveolitis, transverse myelitis, acute hemolytic anemia, macrophage activation syndrome, etc., high-dose hormone shock therapy is often required; acute lupus nephritis, grand mal seizures, acute abdomen due to mesenteric vasculitis, etc., usually require larger doses of hormones; most people with lupus nephritis WHO-III, IV and V require high-dose hormones, daily Prednisone 1mg/kg body weight; lupus nephritis with mild proteinuria (qualitative +~++), obvious rash, plagiocele, etc. usually require only moderate dose hormone, prednisone 0,5mg/kg body weight daily, but if complement C3 <0,3umol/L, high dose hormone is also recommended; if only mild rash or arthritis, only small dose hormone, prednisone 10mg/d is required. These are just examples for reference, and the specific hormone usage needs to be decided according to the patient's condition at the time and the doctor's experience. In the treatment of SLE, hormones are anti-inflammatory agents and immunosuppressants are palliative agents. Therefore, induction therapy for SLE should not rely excessively on hormones, but should be based on immunosuppressants. Intravenous cyclophosphamide (IV-CTX) is the most effective drug for the treatment of severe lupus erythematosus, and the different dose densities are directly related to the intensity of treatment and the near-term side effects (bone marrow suppression and risk of infection). Therefore, the usual dosing regimens of IV-CTX during induction therapy include: 200 mg every other day; 400 mg to 600 mg once a week; 400 mg to 600 mg every other week (European regimen); 1000 mg once a month (US regimen), etc. The choice between these regimens must be determined by fully weighing the pros and cons based on the severity of the disease, the degree of physical tolerance, the degree of risk of infection, etc. Side effects of IV-CTX treatment resulting in hemorrhagic cystitis and bladder cancer are common in Western countries and very rare in China. the long-term side effects of IV-CTX are mainly age and cumulative dose related gonadal toxicity. The advantage of mortifamate (MMF) for SLE is mainly the absence of gonadotoxicity, while the efficacy and risk of infection are comparable to the European and US regimens of IV-CTX [4]. Methotrexate, azathioprine, leflunomide, and rhodopsin preparations are mainly used in mild to moderate SLE or as a follow-up to IV-CTX. Cyclosporine A is also a fast-acting immunosuppressive agent for the treatment of SLE, and is particularly advantageous in reducing proteinuria in lupus nephritis. The rapid rebound of disease on discontinuation is the main disadvantage of cyclosporine A, so it is usually required in combination with methotrexate or CTX. Hydroxychloroquine and thalidomide are more advantageous for skin mucosal damage in SLE. Hydroxychloroquine has outstanding efficacy on heliotrope rash with less side effects, which is suitable for long term treatment of all stages of SLE; thalidomide is effective on oral ulcers of SLE and more effective on discoid erythema. 4, the target treatment should also pay attention to the safety of drugs In the implementation of SLE target treatment, close control is not only concerned about the efficacy, but also the side effects of drugs. Not only should we pay attention to the problem of bone marrow suppression and infection at the beginning of induction therapy, but also to the chronic and long-term side effects of the drugs, because the latter are often neglected and seriously affect the quality of survival of patients. Due to over-reliance on hormones, osteoporosis, femoral head necrosis, and hormonal body type are more common in SLE, and potential side effects such as vascular sclerosis are gradually gaining attention. In fact, in the treatment of SLE, hormones mainly play an anti-inflammatory role, and the induction of remission depends on immunosuppression. This concept needs to be implemented in the process of close control and adjustment of medications in SLE. The gonadal toxicity of cyclophosphamide is related to the cumulative dose, and the cumulative dose of cyclophosphamide required during the IV-CTX induction phase of SLE is usually close to the loading dose for gonadal damage. If the US protocol for IV-CTX treatment of lupus nephritis continues to require that after disease control, shock therapy is continued every 3 months for 2 years, adding another 8,0 g of cyclophosphamide as consolidation therapy is undoubtedly adding to the gonads. The author has been treating severe SLE for more than 10 years, and has been using methotrexate as a follow-up treatment after IV-CTX with satisfactory results. In recent years, European scholars have used methotrexate or azathioprine as a follow-up treatment after IV-CTX, and have also obtained good results. However, there is a lack of randomized controlled trials comparing the efficacy of methotrexate, mortification, and azathioprine. In summary, the treatment of SLE requires the introduction of the concept of goal therapy, induction therapy toward the goal of complete remission, and close control, with adjustments to the treatment regimen based on treatment response and disease regression, to achieve and maintain long-term remission of the disease.