This phenomenon has also been observed in several pathogenic genes related to MASLD, such as transmembrane 6 superfamily member 2,[41] as well as mitochondrial glycerol 3‐phosphate dehydrogenase which was reported by our previous study.[42] Moreover, we found hepatic CD9 inhibition could also impair systemic metabolism and promote fat adipose deposition and obesity via enhancing lipogenesis and weakening thermogenesis of adipose tissue, which indicated the involvement of CD9 in the functional integration between the liver and adipose tissue. This evidence concerns the gene CD9 and obesity due to melanocortin 4 receptor deficiency.