Assuming that inherited mutations will irreversibly lead to cancer in these women, our model of “accelerated geroncogenesis” offers an alternative scenario, testable from a therapeutic point-of-view, where energetic behaviors or new drugs that prevent or revert the pro-tumoral metabolic alterations induced at an early stage by haploinsufficiency of BRCA1/2, could restore metabolic barriers for the processes of genomic instability that occur in the epithelia of these women. This evidence concerns the gene BRCA1 and cancer.