In another study by Groman et al. [13], extensive genetic analysis of the CFTR gene including DNA sequencing of the 27 exons, flanking intronic sequences, and 2 intronic variants known to cause abnormal splicing was performed on 74 patients with “non-classic” CF clinical presentations defined by two or three of the following manifestations of CF: elevated sweat chloride >40 mmol/L, CF lung disease, CF-related gastrointestinal disease, or malformation of the vas deferens. This evidence concerns the gene CFTR and cystic fibrosis.