The BCR-ABL induced CML model demonstrated that the disease progression was significantly slower for the BCR-ABL-Tspan32 transduced BM cell recipients, which was reflected by longer survival times (Supplementary Fig. 1c) and a lower leukemia cell burden in the examined organs (Supplementary Fig. 1d) when compared to that of mice receiving cells with BCR-ABL alone. Here, ABL1 is linked to leukemia.