Since our earlier work revealed a pathogenic role of the CD73/Ado-dependent arm of purinergic signaling in radiation-induced lung fibrosis (49, 50), genetic loss of CD39 with assumed activation of the ATP-dependent proinflammatory arm of purinergic signaling and genetic loss of CD73 with assumed activation of the Ado-dependent anti-inflammatory, repair-promoting arm of purinergic signaling result in opposing outcomes in radiation-induced lung fibrosis. The gene discussed is NT5E; the disease is pulmonary fibrosis.