Comparable results were observed in a murine model of NSCLC-ADC and SCC, where oncogenesis was induced by CRISPR-mediated genome editing of somatic cells by introducing a G12D mutation in the endogenous locus of Kras (K), loss of function mutations in Tp53 (P) and in the tumor suppressors Fbxw7 (F) or Stk11/Lkb1 (L), respectively, which had been published previously [26, 27]. This evidence concerns the gene KRAS and non-small cell lung carcinoma.