Activating PPARγ with rosiglitazone was shown to alleviate the persistent fibrotic phenotype of lesional skin scleroderma fibroblasts [6] and to attenuate inflammation, dermal fibrosis, and subcutaneous lipoatrophy in a murine model of scleroderma [11], suggesting that PPARγ ligands may be considered as potential therapeutic agents for scleroderma. The gene discussed is PPARG; the disease is scleroderma.