Diagnostic Points Diagnosis of such disease, except bone penetrant morphology test except leukemia or non-specific chronic eosinophilic leukemia, need to improve (recommended FISH and PCR testing of bone marrow or peripheral blood) PDGFRA, PDGFRB, FGFR1, JAK2, ABL1, FLT3 gene rearrangement test, KITD816Vc gene (except systemic mast cell hyperplasia) BCR-ABL gene except for lentigo, MPN gene combination except for chronic myeloid accretive neoplasms, except for chronic neutrophilic leukemia (see previous section for diagnosis and treatment details), and except for BCR-ABL-negative atypical lentigo. Flow to look for abnormal immune T-lymphocytes, bone marrow biopsy except for myelofibrosis, and immunohistochemistry for CD117, CD25, and human tryptase. Second-generation gene sequencing is desirable to guide typing, treatment, and prognosis. Common gene mutations Stratified treatment Preferred clinical trials, whether certain types are as long term survivable as lentigenes or must be transplanted, pending clinical trials. Whether second-generation drugs are more effective than first-generation drugs remains to be tested in clinical trials. More types, the first application are required to be combined with 7-10 days of hormone therapy, usually 1mg/kg. If chromosomal normal, FISH detection of PDGFRA positive, the application of imatinib 100mg per day, 3 months after the need for FISH to be reviewed again; if FISH detection of PDGFRA negative, PCR detection of FIP1L1-PDGFRA positive, and also in accordance with the above treatment; if FISH and PCR are negative, treat with hormone or non-specific chemotherapy; whether such patients can survive for a long time like lentigenes is yet to be tested in clinical trials. If there are chromosomal abnormalities, rare PDGFRA rearrangement FISH positive, treatment as above; If there are chromosomal abnormalities, PDGFRB rearrangement FISH positive, apply imatinib 100-400mg per day, but the effect of using 100mg is to be returned by research. Whether the second generation is more effective, pending clinical trials. If there is chromosomal abnormality, FGFR1 rearrangement FISH positive, FISH review, detect TKI targeting FGFR1 kinase mutation, FDA first-line recommended FGFR1,2,3 inhibitor pemetinib; FLT3 inhibitor midostaurin is also recommended as an orphan drug; ponatinib is also recommended as a first-line; first-generation or second-generation TKI drugs have poor efficacy. Such patients are transplanted as early as possible. If chromosomal abnormality, JAK2 rearrangement FISH positive, FISH review PCM-JAK2, other types of JAK2 rearrangement to consider mutation. Leptosine kinase inhibitor combined with JAK2 inhibitor. Early transplantation in such patients. If there are chromosomal abnormalities, FLT3 or ABL1 rearrangement FISH positive, FISH review FLT3 or ABL1 and accompanying gene ETV6, etc., apply lorine kinase inhibitor combined with FLT3 inhibitor. Such patients are transplanted as early as possible. How to treat if the patient has atrial thrombus? The first choice is to exclude thrombophilia, if any, and anticoagulation may be needed for a long time depending on the epidemic. If there is no thrombophilic disease, consider with eosinophil invasion of the heart due to, if eosinophil invasion has been corrected, usually thrombolysis about 3 months can disappear, can stop thrombolytic drugs. Post-infarction ventricular thrombus application of direct oral anticoagulant (DOAC) is more effective than warfarin, but for eosinophil-induced there is no evidence-based medical evidence. If the thrombus has disappeared and the patient still has arrhythmia, or cardiac enzymes are abnormal, or still has symptoms of precordial discomfort, the pathology needs to be excluded from eosinophilic invasion due to myocarditis or cardiomyopathy.