The identification of BIM as a key PTEN-regulated apoptotic mediator in BRAF mutant melanoma cells allowed a novel mechanism of intrinsic drug resistance to be elucidated whereby the paradoxical activation of AKT in PTEN null cells led to a suppression of the nuclear accumulation of FOXO3a and a reduction in BIM mRNA [29]. The gene discussed is BRAF; the disease is melanoma.