Acne is a persistent inflammatory disease of the pilosebaceous unit in which Cutibacterium acnes–induced immune dysregulation has a central function. Retinoic acid receptor-related orphan receptor alpha (RORA), essential transcription factor regulating Th17 differentiation and inflammatory responses via the JAK/STAT pathway, is involved in several chronic inflammatory diseases, suggesting a potential function in acne pathogenesis. This work aims to explain pathogenesis of acne vulgaris, pivotal function of Th17 and its relation to serum level of RORA and its gene polymorphism. The significant elevation of serum RORA protein levels and the predominance of polymorphic RORA genotypes in patients with acne vulgaris suggest an essential function for RORA in acne pathogenesis.