The phosphorylation by CK2 overexpressed in B-ALL depresses Ikaros combining and recruiting HDAC1 to the promoter of BCL2L1, which causes repression of BCL2L1 and increases expression of BCL-XL (Schott et al., 2020). The gene discussed is BCL2L1; the disease is precursor B-cell acute lymphoblastic leukemia.