This is a consequence of the inflammation-induced upregulation and increased activity of CD73 on diverse resident lung cells, as well as immune cells in the normal lung tissue, thus contributing to elevated adenosine levels, presumably to dampen overwhelming inflammatory responses and limit radiation pneumonitis as shown in a murine model of radiation-induced pneumopathy (Wirsdörfer et al., 2013). This evidence concerns the gene NT5E and radiation pneumonitis.