Furthermore, according to a group of studies, patients with NAFLD had a higher level of inflammatory mediators and prothrombotic, including high-sensitive C-reactive protein, tumor necrosis factor α, and interleukin 6, fibrinogen, and plasminogen activator inhibitor that stimulated the nuclear factor-κB (NF-κB) and c-Jun N-terminal kinase (JNK) pathway [45, 46]. This evidence concerns the gene NFKB1 and metabolic dysfunction-associated steatotic liver disease.