A recent study suggests that the suppression of betacellulin is a mechanism responsible for the anti-inflammatory and anti-fibrotic effects of DHA in non-alcoholic steatohepatitis (NASH), with TGFβ-2 and integrins being the main downstream molecular targets of betacellulin [32]. This evidence concerns the gene TGFB2 and metabolic dysfunction-associated steatohepatitis.