Taken together, conditional activation of RAF-1 signaling increased the expression of anti-apoptotic BCL-XL and BCL-2, whereas activation of AKT signaling stabilized anti-apoptotic MCL-1 and prevented the expression of pro-apoptotic BAK. The endpoint of both events is protection of cancer cells to apoptosis executed via the intrinsic pathway of caspase activation [39]. The gene discussed is BCL2; the disease is cancer.