Finally, targeting the intergenic GSH sites Dep.3 and Ap.102 resulted in downregulation of the AML-associated proto-oncogene FLT3 (0.44, p ≤ 0.0014) and overexpression of INHBA (18.4-fold change, p ≤ 0.005) (Figure 3C). The gene discussed is INHBA; the disease is acute myeloid leukemia.