In normal alveoli, surfactant secretion is controlled by extracellular ATP and other nucleotides (Praetorius and Leipziger 2009), however, under pathological condition, overloaded ATP remains a major endogenous signal in promoting the release of pro-inflammatory cytokine IL-1β via activation of NLRP3 inflammasome through the binding of P2X7R receptor, thereby facilitating lung fibrosis progression (Gicquel et al. 2017; Riteau et al. 2010). The gene discussed is NLRP3; the disease is pulmonary fibrosis.