Their study further provides experimental evidence that VEGF is increased during the transition from steatosis to NASH in a mice model fed on MCD diet, while inhibition of VEGF receptors (VEGFR2) arrested the development of NASH by downregulating genes involved in inflammatory response such as tumor necrosis factor-α (TNF-α), interleukin-1b (IL-1b). This evidence concerns the gene VEGFA and metabolic dysfunction-associated steatohepatitis.