Consistently, in the present study, we observed that the deletion of MBOAT7 or TM6SF2 alone and mainly together promoted fission while inhibiting both fusion and mitophagy, showing unbalanced mitobiogenesis and an increased assembly of misshapen and failed organelles as we recently demonstrated in the hepatic biopsies of MASLD patients stratified according to their genetic background [41]. This evidence concerns the gene MBOAT7 and metabolic dysfunction-associated steatotic liver disease.