Genetic models also support an anti-neoplastic role for PPARγ: mice hemizygous for germline PPARγ exhibit an increase in spontaneous skin cancers while mice conditionally lacking epidermal PPARγ (Pparg-/-epi mice) exhibit a marked increase in both chemical and ultraviolet B (UVB)-induced carcinogenesis [13,14,15]. The gene discussed is PPARG; the disease is skin cancer.