In summary, our and other’s results pointed to a regulatory window for the expression level of SHIP1, which depends partly on Ikaros and must neither be undercut (e.g., in T-ALL and CML) nor exceeded (e.g. in Ph-positive B-ALL and ETV6-RUNX1-positive B-ALL). The gene discussed is RUNX1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.