Based on the pathways findings in NoSTox subjects, we hypothesized that functional impairment in the control of the radiation-induced expression of NF-kB, mainly in/of the ubiquitination/deubiquitination mechanisms, together with an impairment of the AIM2 inflammasome pathway and a dysregulation of the insulin-like growth factor (IGF) axis (possibly correlated to a impaired plasmalogen biosynthesis), could modulate radiation-induced lung inflammation preventing development of acute radiation pneumonitis and chronic radiation-induced pulmonary fibrosis (Figure 1). This evidence concerns the gene IGF1 and inflammation.