Although our results implicate GCN2 as the potential factor determining ALL translational repression, given its rescue when GCN2 is inhibited (Fig. 4i), the lack of any selective increase in eIF2α phosphorylation under adipocyte conditions (Supplementary Fig. 4v) together with no orthogonal features of activated ISR downstream (Fig. 4d and Supplementary Fig. 4v-w) as well as incomplete phenotype reversal despite potent eIF2α inhibition would argue against this factor being the principal driver. The gene discussed is EIF2AK4; the disease is acute lymphoblastic leukemia.