Clinically, the targeting and elimination of LSCs are essential for CML elimination.4,5 Strikingly, we found that high Tspan32 expression also suppressed LSC proliferation and impaired their function (Fig. 4), which suggested that targeting Tspan32 network might offer a potential strategy for LSC elimination. The gene discussed is TSPAN32; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.