TNF-α, for example, is present in the physiopathology of MAFLD due to the activation of pro-inflammatory macrophages during the pathological hypertrophy of adipocytes, promoting lipolysis and contributing to insulin resistance by acting on the insulin receptor and inducing the phosphorylation of Ser307 instead of tyrosine on Irs 1 [19,39]. This evidence concerns the gene INSR and Insulin resistance.