To explain these results, we suggest that the FABP12-PPARγ pathway plays a dual role in directing energy metabolic adaptation to support metastatic transformation of PCa cells, by stimulating mitochondrial oxidation for ATP production, and triggering processes such as epithelial-to-mesenchymal transition (EMT), cell motility and invasion, that increase ATP consumption [29]. This evidence concerns the gene FABP12 and posterior cortical atrophy.