BCL2 and glioblastoma: The activation of AMPK promoted p53 activation, leading to the inhibition of mTORC1 signalling, and modified the expression levels of apoptosis-related proteins such p21, Noxa, BAX, and BCL-2, which all contributed towards TMZ-induced glioblastoma cell apoptosis, which was very similar to our findings (Zhang et al., 2010).