We demonstrated that increased TIGAR level inhibited the expression of PFKFB3 protein in vitro (Fig. 4G) and in vivo (Fig. 5F), implying that decreased glycolysis was mainly due to reduced PFKFB3 in T-ALL with impaired miR-652-5p, and overexpressed TIGAR would repress glycolysis via the crosstalk between TIGAR and PFKFB3. The gene discussed is TIGAR; the disease is acute lymphoblastic leukemia.