TGFB1 and metabolic dysfunction-associated steatohepatitis: In the pathophysiological mechanisms involved in MAFLD and NASH should be considered the elevation of oxidant molecules, fibrogenic mediators as transforming growth factor beta-1 (TGF-β1), insuline-like growth factor (IGF-1) and endothelin-1, inflammatory mediators as C-reactive protein (CRP), interleukin (IL)-6 and tumor necrosis factor (TNF)-α and pro-coagulant factors as fibrinogen, factor VIII, and plasminogen activator inhibitor-1 [24].