Bcl-w is up-regulated also through pathways besides the Akt one: Tran et al. demonstrated that Bcl-w can be up-regulated via the NFkB pathway activated by TWEAK (tumor necrosis factor-like weak inducer of apoptosis) through stimulation of its receptor, Fn14; moreover, the TWEAK-Fn14 pathway can induce survival of glioma cells, at least in part by up-regulating the quantity of Bcl-w protein [40]. The gene discussed is AKT1; the disease is central nervous system cancer.