In fact, overexpression of yeast‐derived NDI1 in mammalian cells has been employed as a therapeutic strategy to rescue mitochondrial dysfunction caused by rotenone inhibition or mutations in mammalian complex I genes.[32] Martínez‐Reyes et al. demonstrated that NDI1 overexpression can compensate for mitochondrial complex I deficiencies, thereby promoting tumor cell growth.[14] Notably, previous studies have reported that COA4 participates in regulating mitochondrial COX activity of S. cerevisiae. This evidence concerns the gene AVPR2 and neoplasm.