Two independent studies in metastatic patients and in those with surgically resected NSCLC are in favor with the idea that different codon variants may promote activation of distinct transcriptional networks which impact on prognosis and/or therapeutic susceptibilities: KRASG12C or KRASG12V positivity was associated with worse disease-free and overall survival when compared with other KRAS variants or wildtype protein, at least partly due to increased levels of epithelial to mesenchymal transition genes and lower levels of genes predicting KRAS dependency [28,29]. The gene discussed is KRAS; the disease is non-small cell lung carcinoma.