Our results imply that serum deprivation increases responsiveness to GLI1/2 targeting agents in T-ALL cells possibly through increased stability of GLI1 protein determined by augmented S6K1-mediated S84 phosphorylation [26] and decreased AMPK-dependent S408 (and possibly S104, S1074) phosphorylation [19,20]. Here, GLI1 is linked to acute lymphoblastic leukemia.