In human K562 chronic myeloid leukemia (CML) cells, IGF2BP3 enhanced cell survival following ionizing radiation (IR) therapy by binding to IGF2 mRNA, whereas IGF2BP3 knockdown inhibited cell proliferation, suggesting potential use of IGF2BP3 as a novel drug target for promoting CML sensitivity to IR therapy (39). The gene discussed is IGF2BP3; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.