The pathobiology of primary cicatricial ("scarring") alopecia (PCA) remains poorly understood and underinvestigated. In this issue, Karnik et al. identify a previously unsuspected player, peroxisome proliferator-activated receptor-gamma (PPARgamma), in the pathogenesis of the most frequent form of PCA, lichen planopilaris (LPP). The authors show that PPARgamma is required for maintenance of a functional epithelial stem cell compartment in murine hair follicles, that the targeted deletion of PPARgamma in the bulge/isthmus area of the hair follicle epithelium generates a skin pathology that resembles LPP, and that LPP patients show gene expression changes that indicate a defect in lipid metabolism and peroxisome biogenesis. This study invites the revisitation of many open questions in PCA pathobiology and the exploration of new avenues for future PCA management.