It has also been suggested that the proinflammatory cytokines interleukin-6 (IL-6), interleukin-1beta (IL-1β), and tumor necrosis factor-alpha (TNF-α), as well as decreased plasma adiponectin concentrations resulting from increased or dysfunctional visceral adipose tissue, may not only be involved in the development and progression of NAFLD through effects on glucose and lipid metabolism and insulin resistance but may also affect the coronary arteries and cause HF [29, 30]. This evidence concerns the gene IL1B and metabolic dysfunction-associated steatotic liver disease.