Importantly, in some B-ALL and T-ALL cell lines and cells derived from patients with B-ALL, reduction of the glycolytic rate using 2-deoxy-D-glucose (2-DG), lonidamine (LND), or 3-bromopyruvate (3-BrPA), can restore the sensitivity of these cells to glucocorticoids (Hulleman et al., 2009; Gu et al., 2017); and the combined treatment of a glycolytic inhibitor in conjunction with the silencing of anti-apoptotic proteins such as myeloid cell leukemia sequence 1 protein (MCL-1) can enhance the antitumor activity in cells resistant to prednisolone (Ariës et al., 2013). Here, MCL1 is linked to acute lymphoblastic leukemia.