Acne vulgaris is a chronic inflammatory dermatosis of the pilosebaceous unit driven by four pathogenic factors: androgen-mediated sebaceous gland hyperactivity (increased sebum production under influence of dihydrotestosterone converted from testosterone by 5-alpha reductase in sebaceous glands), follicular hyperkeratinization (abnormal keratinization of the follicular infundibulum creates the microcomedo -- the precursor lesion), Cutibacterium acnes colonization (anaerobic bacterium that thrives in the lipid-rich, oxygen-poor environment of the obstructed follicle, producing lipases that generate pro-inflammatory free fatty acids and activating toll-like receptor 2 and inflammasome pathways), and inflammation (innate and adaptive immune responses to C. acnes and follicular rupture). The clinician classifies acne severity to guide treatment: mild (comedonal -- open and closed comedones with few inflammatory papules, treat with topical retinoid plus or minus benzoyl peroxide), moderate (papulopustular -- numerous papules and pustules, add topical antibiotic such as clindamycin always combined with benzoyl peroxide to prevent resistance), and severe (nodulocystic -- deep painful nodules, cysts, risk of scarring, consider oral isotretinoin or referral to dermatology). The clinician prescribes isotretinoin understanding its mechanism (reduces sebaceous gland size and sebum production by 80%, normalizes...