Therefore, further studies should better investigate these mechanisms and, in particular, address whether: (1) fatty acids are involved in the pathogenesis of this effect of HFD, (2) increased degradation of OXPHOS subunits might contribute to reduced OXPHOS activity, (3) NADPH oxidase is responsible for the HFD-induced nitro-oxidative stress, (4) inhibition of NADPH oxidase prevents OXPHOS dysfunction and nonalcoholic steatohepatitis, and (5) fatty acids are able to activate this oxidase. Here, FMO5 is linked to metabolic dysfunction-associated steatohepatitis.