Moreover, inflammatory mediators like IL-6 and TNF-α plays an essential role in the development of NAFLD in human and key stimulus for production of various proteins in the liver (e.g., fibrinogen, high-sensitivity C-reactive protein) in acute-phase of response; where a higher level of high-sensitivity C-reactive protein (hs-CRP) indicates an increased risk of cardiovascular disorder (CVD) in a patient with NAFLD mediated NASH [187]. This evidence concerns the gene IL6 and metabolic dysfunction-associated steatotic liver disease.