As PARK2 deficiency results in both increased inflammation and genomic instability [37–39], we assessed a potential role of PARK2 in lung cancer and COPD through a comprehensive validation study of 114 informative single nucleotide polymorphism (SNP) variants of PARK2 (Supplementary Table S2) in 2,484 cases and controls with well-defined lung cancer (LC) and COPD phenotypes (Table 1). Here, PRKN is linked to laryngotracheoesophageal cleft.