Choi et al. [71] revealed that leptin promoted the phenotypic transition of HSCs by activating the Hh pathway followed by the development of liver fibrosis, that is, by the activation of the PI3K/AKT and JAK/STAT signaling pathways via binding to ObR (leptin receptor) followed by the activation of Hh pathways which also induce osteopontin leading to fibrosis progression in NASH [102]. This evidence concerns the gene LEPR and metabolic dysfunction-associated steatohepatitis.