Acne is a chronic inflammatory skin disease of the follicular sebaceous glands with a prevalence of 70% to 87% and a psychological and social impact on adolescents that exceeds that of asthma and epilepsy. Treatment options for acne vary widely among clinicians, with some treatments having uncertain efficacy and lacking evidence-based support, and individual approaches even causing damage to patients. Therefore, it is essential to develop a set of proven guidelines for the treatment of acne to standardize its treatment. Of course, guidelines are not static and need to be updated regularly as new evidence-based medicine and new drugs are developed. This guideline is based on the acne guideline published in 2008, and has been revised based on user feedback and domestic and international acne research progress. 1. Pathophysiology of acne Acne is a chronic inflammatory disease of the sebaceous units of the hair follicles, and the pathogenesis of acne is still not fully understood. Genetics, androgen-induced sebum secretion, follicular sebaceous duct keratinization, Propionibacterium acnes colonization, inflammation, and immune response are all factors that may be involved. The rapid development of sebaceous glands and lipid secretion under the influence of androgens are the pathophysiological basis of acne. The development of adrenal and gonadal glands after puberty leads to increased secretion of androgen precursors such as dehydroepiandrosterone sulfate (DHEAs), which are converted to active dihydrotestosterone by a series of androgen metabolizing enzymes such as 5a-reductase. The enhanced expression or activity of androgen receptors or related androgen metabolizing enzymes in the skin in a genetic background is also an important factor contributing to sebaceous gland hypersensitivity to androgens and lipid overproduction. In addition, there are changes in the lipid composition of sebum in acne patients, such as increased content of peroxisqualene, wax esters, free fatty acids, increased proportion of unsaturated fatty acids, and decreased content of linoleic acid. Abnormal keratinization of the follicular sebaceous ducts is another important factor in the development of acne and a major pathological phenomenon. Keratinization of epithelial cells leads to blockage of the follicular sebaceous ducts and impairment of sebum drainage, resulting in microcomedema visible under the microscope and acne visible to the naked eye. Propionibacterium acnes is closely related to the development of acne. The formation of microcomedones and acne creates a favorable local environment for the proliferation of Propionibacterium acnes, which has anaerobic growth characteristics. It is thought that P. acnes may be involved in the development of acne inflammation through natural immunity, acquired immunity, and direct induction. In early acne, inflammation may be caused by a natural immune response mediated by Toll-like receptors (TLR), which induces the release of proinflammatory factors, especially IL-1a. In the later stages of the disease, the hair follicle wall breaks down and lipids and hairs from the follicle enter the dermis, further aggravating the inflammatory response. The grading of acne is an important basis for acne treatment and efficacy evaluation. Whether acne is graded according to the number of lesions or the nature of the lesions, the treatment options are basically the same. For clinical convenience, this guideline classifies acne into 3 and 4 grades based on the nature of the lesions: mild (grade I): acne only; moderate (grade II): inflammatory papules; (moderate grade III): pustules; and severe (grade IV): nodules and cysts.