Our retrospective study of lung cancer patient tissues corroborates the in vitro findings to enable molecular precision in defining PKR and OAS as critical tumor-suppressors of lung carcinogenesis (Figure 7B,C), and that their deficiency, as observed in the later stages of lung cancer patient tissues, likely provoked the advancement of the disease (Figure 7B,C). This evidence concerns the gene EIF2AK2 and lung carcinoma.