N−3 PUFAs can inhibit inflammatory mediators, such as protein kinases (c-jun N-terminal kinases, MAPK, p38), nuclear factor κB, and cytokines (tumor necrosis factor-α, interleukin (IL)−1β, IL−6, etc.), and reduce lipid biosynthesis by down-regulating sterol regulatory element binding protein 1c in several metabolic diseases [43]. This evidence concerns the gene WEE1 and Other metabolic disease.