Fig. 1

Emergence of a CSF3R-mutant, neutrophilic leukemia during targeted therapy for BCR-ABL1. Hematologic toxicity and the emergence of treatment-resistant clones shaped this CML patient’s clinical course. Ultimately, treatment with ponatinib successfully controlled the BCR-ABL1 clone, while another neutrophilic clone containing CSF3R mutations, but not BCR-ABL1, expanded