More recently, Nolan and colleagues have also shown the potential of RANKL as a therapeutic target in a Brca1-deficient mouse model, while in normal breast tissue of BRCA1-mutation carriers, identifying luminal RANK(+) progenitors that are highly proliferative and bear a molecular signature similar to that of basal-like BC, this indicates RANKL inhibition as a promising strategy in the prevention setting [72•]. This evidence concerns the gene BRCA1 and breast cancer.