Recently, it was demonstrated that ATP-P2X7-inflammasome-caspase 1-IL-1/18 axis played a role in smoke-induced airway inflammation in healthy smokers or COPD patients as well as murine COPD models, with increased activation of P2X7 receptor/caspase 1 and elevated IL-1β and IL-18 levels (56). The gene discussed is IL18; the disease is chronic obstructive pulmonary disease.