The respiratory exposure of silica NPs induces hepatotoxicity; the authors [45] focused on the role of SiNPs in the pathogenesis and progression of NAFLD and demonstrated a significant aggravation of hepatic steatosis, inflammation, and collagen deposition in ApoE−/− mice, along with high concentrations of ALT, AST, and LDH levels associated with liver damage [45]. This evidence concerns the gene APOE and metabolic dysfunction-associated steatotic liver disease.