Reconstitution of wild-type variants of IKZF1 or PAX5 in primary B-ALL cells caused downregulation of several glucose transporters (GLUT1, GLUT3, and GLUT6) and glucose utilization effectors (hexokinase 2/3, HK2/3; glucose-6-phosphate dehydrogenase, G6PD), paralleled by the upregulation of direct and indirect glucose transport inhibitors (nuclear receptor subfamily 3 group C member 1, NRC3C1; thioredoxin-interacting protein, TXNIP; cannabinoid receptor type 2, CNR2), leading to energy crisis and cell death [13]. Here, TXNIP is linked to precursor B-cell acute lymphoblastic leukemia.