Pro-inflammatory cytokines, e.g., interleukin-6 and TNF-α, which are overexpressed in NAFLD, attenuate mediated signaling through the activation of various stress-related protein kinases, including Jun N-terminal kinase (JNK) and inhibitor kappa beta kinase (IKK) [19]. This evidence concerns the gene TNF and metabolic dysfunction-associated steatotic liver disease.