Increased local and systemic inflammation and fatty acid (FA) availability and the dysregulation of insulin and growth factor (GH), the insulin-like growth factor (IGF)-1 axis, sex steroid hormones, and adipokine synthesis and secretion [12] have emerged as possible mechanisms that could underpin the complex and intricate crosstalk between PPAT and PCa. This evidence concerns the gene IGF1 and posterior cortical atrophy.