To clarify the functional roles of VDR in the progression of BCR::ABL1-driven CML, we utilized a VDR knockout (KO) mouse model, in which VDR deficiency was confirmed by the undetectable expression of VDR in BM cells compared to the wild-type (WT) control (Supplementary Figure S4A and B). The gene discussed is VDR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.