Mice expressingconstitutively active VP16-PPARγ in the mammary gland did not exhibit atumorigenic phenotype but accelerated tumorigenesis when crossed withMMTV-polyoma middle-T antigen mice [40], intimating that theunliganded receptor may have interfered with tumor suppressor transactivationby endogenous PPARγ through corepressor recruitment. This evidence concerns the gene PPARG and neoplasm.