These data suggest that the NOD2 2722G > C variant was not sufficient to trigger pulmonary sarcoidosis by itself and it is the presence of other variants (IL17RA 958 T > C, EPHA2 2875G > A and KALRN 28C > T) that contribute to the pathology in patients with pulmonary sarcoidosis of family X, perhaps by enhancing the development and chronicity of pulmonary sarcoidosis in family X. The gene discussed is KALRN; the disease is pulmonary sarcoidosis.