BCL2 and glioblastoma: VILIP3 was shown to suppress cancer progression by promoting p21 stabilization,31 whereas other studies reported that VILIP3 promotes glioblastoma cell proliferation.19 Here, we provide the first evidence showing that the VILIP3 protein is a new catalytic substrate protein of NMT1 and that myristoylation of VILIP3 affects its stability to activate the NFκB/Bcl-2 regulatory axis.