BCL2 and breast carcinoma: In a study of breast cancer cell populations exposed to hyper-fractionated radiation therapy, Hein et al. reported that RAC1 inhibition in a radiation therapy-resistant breast cancer population led to a decreased activity of ERK1/2 and NF-κB, decreased expression of anti-apoptotic Bcl-2 family proteins, and decreased expression of Poly (ADP-ribose) polymerase (PARP), suggesting the induction of apoptosis [6].