Genetic variants in the FADS1 and FADS2 gene clusters have been associated with altered (n-6) and (n-3) PUFA metabolism [47, 48], whereas metabolic disorder in PUFA exerted effects on PCa by mediating the formation of eicosanoid inflammatory mediators (prostaglandins, leukotrienes, thromboxanes, and lipoxins), angiogenesis, immune cell regulation, and membrane structure and function [49, 50]. Here, FADS2 is linked to posterior cortical atrophy.