JNK or p38 agonists could partly rescue the down-regulation of migration, invasion, and foci formation by ZDHHC17 knockdown, whereas both p-JNK and p-p38 inhibitors could suppress the ZDHHC17-overexpressed tumorigenic and invasive phenotype (Figures S11A-S11C), demonstrating that these traits of ZDHHC17-expressing GBM cells are related to JNK and p38 activation. This evidence concerns the gene MAPK8 and glioblastoma.