Even more important, own previous work on the pathogenic role of CD73 in radiation-induced lung fibrosis in mice (49, 50) suggests that pharmacologic strategies inhibiting CD73-dependent accumulation of Ado might be suited to improve the therapeutic ratio of RT by influencing both tumor-promoting and fibrosis-promoting effects of CD73/Ado signaling in irradiated tumor and normal tissues. The gene discussed is NT5E; the disease is neoplasm.