Another transcriptomics-based study, including NAFLD patients with and without the PNPLA3 I148M genetic risk variant, identified a similar robust up-regulation of IL-32 in individuals with a severe phenotype (defined as NAFLD activity score ≥ 4, fibrosis stage ≥ 2, or presence of steatohepatitis), independently of the underlying genotype. This evidence concerns the gene IL32 and metabolic dysfunction-associated steatotic liver disease.