PNPLA3 and steatosis: In case of I148M protein variant, the reduction of PNPLA3 hydrolytic efficiency decreases the hydrolysing of n-9 fatty PUFAs, leading to an n-6 overload and two critical consequences: the TG synthesis with increased hepatocyte overload and the production of n-6 pro-inflammatory-derived species (e.g., AA), worsening the steatosis and promoting NASH [141,142] (Figure 3).