On the contrary, loss-of-function variants on the hydroxysteroid (17-beta) dehydrogenase-13 (HSD17B13) gene, such as the rs72613567, have been proposed to mitigate NAFLD’s progression to NASH, fibrosis, and hepatocellular carcinoma (HCC) by the loss of its enzymatic activity, which leads to increased retinol–binding protein (RBP4)–transthyretin (TTR) transport from hepatocytes [18,30,31,32]. This evidence concerns the gene TTR and metabolic dysfunction-associated steatohepatitis.