A number of recent studies have revealed a pro-apoptotic role for NF-κB signaling [23]–[25], and together with our recent observations indicating that prolonged exposure of medulloblastoma cells to CFM-4 also resulted in NF-κB activation that likely serves to potentiate/support apoptosis [20]; we investigated the extent CFMs also regulated NF-κB signaling in MPM cells. This evidence concerns the gene NFKB1 and medulloblastoma.