To investigate the role of ATF4-dependent fructolysis in GBM growth, we intracranially injected luciferase-expressing U87 cells without or with ATF4 KO (Fig. 4e) or ATF4 binding-deficiency in the promoters of SLC2A5 or ALDOB (Fig. 4f) into athymic nude mice. Here, SLC2A5 is linked to glioblastoma.