[14] The overproduction of IL-17 and activation of Th17 cells have been demonstrated to underlie the development of acne.[15]Cutibacterium acnes phylotype IA1 via Toll-like receptor 2-dependent signaling, to trigger the production of IL-6, IL-8, transforming growth factor-β, IL-1β and induces CD4 lymphocytes differentiate into Th17 lymphocytes.[16] The virulence profile of Cutibacterium acnes is associated with alterations in the microenvironment of the bacterium located within the pilosebaceous follicle. The gene discussed is CD4; the disease is acne.