A crucial point is the decrease of TNF-α, a key factor in the development of Non Alcoholic Fatty Liver Disease (NAFLD) and Non Alcoholic Steato Hepatitis (NASH) [34], of IL-6, hepatoprotector in liver steatosis by reducing oxidative stress [35], of IL-10 [36] and of IL-17A, implicated in both regulation of obesity and NAFLD [37]. Here, IL17A is linked to metabolic dysfunction-associated steatohepatitis.