In addition, we demonstrated that BV6 primes glioblastoma cells in a RIP1-dependent manner for Temozolomide (TMZ), the first-line chemotherapeutic agent in the treatment of glioblastoma, since knockdown of RIP1 significantly reduced BV6- and TMZ-induced caspase-8 activation and apoptosis [17]. Here, CASP8 is linked to glioblastoma.