In prostate cancer cells, PPARγ stimulates AKT serine/threonine kinase 3 (AKT3) expression, which favors PGC1α localization to the nucleus, mitochondrial biogenesis, and elevates ATP levels, ultimately leading to tumor-cell proliferation and metastasis via an enhanced epithelial–mesenchymal transition [350]. This evidence concerns the gene PPARG and neoplasm.