However, it is reasonable to suggest that the tumor suppression function afforded by the mitochondrial dose of IF1 in these types of carcinomas also depends on the nuclear reprogramming exerted by the activation of specific kinases and transcription factors mediated by mtROS signaling generated as a result of the IF1-mediated inhibition of the ATP synthase (Figure 3). This evidence concerns the gene ATP5IF1 and neoplasm.