C-MYC signal transduction is associated with NAFLD-related fibrosis.[37] The specific reduction of MYC in the mouse intestine can improve HFD-induced obesity, insulin resistance, liver steatosis, and steatohepatitis.[38] Peroxisome proliferator-activated receptor-γ (PPARγ) is involved in the NAFLD pathogenesis via adipogenesis, insulin resistance, inflammation, and oxidative stress.[39] HSP90AA1 is a common subtype of HSP90. This evidence concerns the gene HSP90AA1 and metabolic dysfunction-associated steatotic liver disease.