Studies on cells from patients with T-ALL have indicated that HDAC4 knockdown is associated with increased sensitivity to prednisone.26,28 In addition, HDAC4 causes stimulation of HIF-1 (hypoxia-inducible factor-1), enhancing the tumorigenesis process in patients with T-ALL (Table 1) (Figure 2.B).29 This evidence concerns the gene HDAC4 and acute lymphoblastic leukemia.