These results suggest a positive feedback loop regulation between ERK1/2 signaling and BRCA1 protein stability in response to IR, which may play an important role in sustaining the G2/M cell cycle checkpoint response following IR, as inhibition of either BRCA1 or ERK1/2 in breast cancer cells abolishes G2/M cell cycle arrest and results in a concomitant induction of apoptosis [72]. This evidence concerns the gene BRCA1 and breast carcinoma.