It can also increase the expression of P53 and its transcriptional target P21, finally leading to the arrest of the GBM cell cycle in the G2/M phase, causing mitochondrial dysfunction, consequently releasing Cyt-C, activating caspase 3/9, and inducing mitochondrial apoptosis (Zheng et al., 2021). Here, CASP3 is linked to glioblastoma.