Early finding has shown that the increased expression of HMGB1 in samples that derived from patients with CF and from a murine model of CF lung disease (Scnn1b-transgenic [Scnn1b-Tg] mouse) is directly chemotactic for neutrophils through a C-X-C chemokine receptor (CXCR)-dependent mechanism, while intratracheal instillation of HMGB1 in mice triggers neutrophil influx and contributes to lung matrix degradation [53]. This evidence concerns the gene SCNN1B and lung disorder.