Robledo-Avila et al. in their study suggested that, in CF neutrophils, the increased intracellular concentrations of Ca2+ may be affected by CFTR malfunction through the involvement of the transient receptor potential (TRP) Ca2+ channels, which allow the influx of Ca2+ from the extracellular compartment, with consequent diminished NADPH oxidase response and impaired secretion of NETs [73,86]. The gene discussed is CFTR; the disease is cystic fibrosis.