However, in this context, it has to be considered the presence of both a truncated splice variant of human PPAR-α that negatively interferes with wild-type PPAR-α activity [24] and polymorphic variants in the functional coding sequence of human PPAR-α, val227ala, and Leu162Val, which are implicated in NAFLD and IR but not with liver damage, respectively [25, 26]. This evidence concerns the gene PPARA and metabolic dysfunction-associated steatotic liver disease.