CD36 and metabolic dysfunction-associated steatotic liver disease: In animal studies, the mouse model of HFD-induced NAFLD has been shown to have an increased abundance of Desulfovibacteriaceae.[36,37] In humans, it has also been reported that BMI and Desulfovibrio are positively associated in overweight subjects.[38] Mechanistically, a study found that in HFD-induced mice, Desulfovibrio piger increases intestinal permeability and the expression of the scavenge receptor CD36 in the liver, which contributed to the development of NAFLD.[39] Our results provide genetic evidence to support the causal role of these gut microbiota in NAFLD.