Data on the interaction between the BCR::ABL1 clone and CALR clone commonly showed an inverse relation as BCR::ABL1 decreased under TKI therapy, whereas the CALR-mutant clone persisted, often with a high allele burden, during the disease course despite successful TKI treatment of CML. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.