Recent European GWAS have identified a series of SNPs [MERTK (rs4374383), TULP1 (rs9380516), GLT8D2 (rs2629751), and RNF7 (rs16851720)] as susceptible genetic alterations for HCV-related liver fibrosis[12], and other studies have proposed SNPs at rs738409 in adiponutrin/patatin-like phospholipase domain-containing 3 (PLPNA3) and rs5764455 in PARVB, which is in strong linkage disequilibrium with PLPNA3, as genetic determinants of liver fat content[13], disease progression, and fibrosis in nonalcoholic fatty liver disease (NAFLD)[14,15,16,17,18,19,20]. This evidence concerns the gene PARVB and metabolic dysfunction-associated steatotic liver disease.