We previously developed a series of (l-)monobodies directed to the Src homology 2 (SH2) domain of BCR::ABL1, which resulted in inhibition of BCR::ABL1 activity, signaling and leukemogenesis in CML cells through different mechanisms-of-action10,11,13. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.