Acne vulgaris (AV) is a common chronic inflammatory skin disorder of the pilosebaceous unit among adolescents and is characterized by comedones, papules, pustules, and nodules. 1 The pathogenesis of AV involves a complex multifactorial process, including altered sebum secretion, excessive follicular keratinization, Propionibacterium acnes (P. acnes) proliferation, neuroendocrine dysregulation, and inflammation. 2,3 Additionally, genetic involvement has already been confirmed by multiple twins-based and family-based studies on acne. 4 Acne can cause disfigurement and related psychological comorbidity on patients. 5 Despite being a common disease, the treatment of acne is still tricky and unsatisfactory. To seek better treatment strategies, a comprehensive understanding of the molecular mechanism underlying the development of AV is urgent.Single-nucleotide polymorphisms (SNPs) of genes refer to the substitution of a single nucleotide at a specific position in the