Functional analysis of E2F1 in the CD133(+) melanoma subpopulation demonstrated that overexpression of E2F1 induced both degradation of the antiapoptotic protein Mcl-1 and activation of the ASK1/JNK and p38 pathways, which are involved in regulating the localization of Bax to mitochondria to trigger apoptosis (76) (Figure 2A). The gene discussed is PROM1; the disease is melanoma.