PPARγ overexpression reduced breast cancer cell growth in xenograft models, and was associated with increased autophagy and the inhibition of angiogenesis; meanwhile, overexpression in stromal cells enhanced tumor growth, which has been related to the increased expression of autophagic markers, the production of lactate, cell hypertrophy, mitochondrial dysfunction, and senescence, as illustrated by higher p16/p21 expression and beta galactosidase [166]. This evidence concerns the gene CDKN2A and neoplasm.