The possible mechanism is that both NAFLD and T2DM are associated with a state of systemic hypo-inflammation, which may encourage atherosclerosis through the secretion of various cytokines such as interleukin-6, interleukin-1, tumor necrosis factor-α, and acute phase proteins (C-reactive protein, fibrinogen, and fetal protein-A) (31). Here, IL6 is linked to metabolic dysfunction-associated steatotic liver disease.