To determine impact of specific mutations in KD BCR::ABL1 and leukemia-associated genes on asciminib resistance in our in vitro model of naturally mutated CML myeloblasts and to investigate treatment options including combinatory therapy in vivo, based on our previous results [5], IC50 values for asciminib, ponatinib, and venetoclax were assessed in each individual clones followed by 48 h of drug exposure. The gene discussed is BCR; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.