Finally, in addition to their role for the development of ALI, P2XR7 and P2XR4 activation was shown to assume major importance for CS-related lung injury: CS exposure caused up-regulation of both the P2XR4 and P2XR7 [49], and either pharmacological blockade or genetic deletion of the P2XR7 attenuated the pulmonary IL-1β and IL-18 accumulation after CS exposure [50]. The gene discussed is IL18; the disease is acute respiratory distress syndrome.