Cystic fibrosis (CF) is caused by mutations in the CFTR gene, which encodes a chloride and bicarbonate ion channel (1). Among the approximately 150 known disease-causing mutations in CFTR, deletion of the phenylalanine-508 codon (DeltaF508) is the most common and results in protein destabilization, misfolding and ultimately degradation (2). Although the most pronounced lung disease symptoms of CF, including chronic bacterial infection and purulent airway obstruction, are highly associated with neutrophils, the lack of cellular models for CF neutrophils has hindered progress in understanding the significance of these cells for CF pathogenesis (3).The HL-60 DeltaF508-CF human promyelocytic cell line is a derivative of the HL-60 promyelocytic leukemia cell line that has been edited via CRISPR/Cas9 technology for homozygous deletion of CFTR F508 (3). Differentiation of HL-60 DeltaF508-CF cells into neutrophils occurs upon treatment with DMSO. Differentiated HL-60 DeltaF508-CF cells demonstrate normal levels of CD11b staining but substantially reduced CFTR surface expression compared to differentiated HL-60 control cells, in addition to compromised bactericidal activity (3). Source:The HL-60 DeltaF508-CF human promyelocytic cell line was derived from HL-60 promyelocytic leukemia cells transfected with a hCFTR-Cas9-eGFP plasmid. Single-cell clones were sorted for eGFP expression and screened for homozygous deletion of CFTR F508 via nuclease digestion and DNA sequencing (3).