Interestingly, a recent case study described a NASH patient carrying a heterozygous MUL1 mutation, which led to the accumulation of dysfunctional mitochondria; this condition was mitigated by SGLT2 inhibitor treatment (50 mg of ipragliflozin) by activating residual MUL1 activity in this haploinsufficiency [122]. This evidence concerns the gene MUL1 and metabolic dysfunction-associated steatohepatitis.