Furthermore, genes upregulated in the mutant-KRAS-specific signature contained oncogenes involved in many human cancers, whose expression is often associated with poor prognosis (Human Protein Atlas, www.proteinatlas.org37 and38–41) and/or resistance to therapy, such as the membrane protein Plac8. Noteworthy, its upregulation causes NSCLC resistance to the tyrosine-kinase inhibitor Osimertinib52 and its silencing in renal cell carcinomas significantly increases their sensitivity to Cisplatin53. This evidence concerns the gene KRAS and hereditary clear cell renal cell carcinoma.