HRAS and nonpapillary renal cell carcinoma: These are N-Ras proteins containing Cys-Val-Val-Met, K-Ras4a with Cys-Ile-Ile-Met, K-Ras4b with Cys-Val-Ile-Met, and H-Ras with Cys-Val-Leu-Ser.39 Indeed, FTIs were first devised to inhibit Ras, however, alternative prenylation of K- and N-Ras hinders these drugs’ ability to affect Ras oncogenes.40 Furthermore, clinical effects of FTIs do not appear to be linked to Ras mutations or inhibition of Ras effectors.41 Also, our CRISPR/Cas9-based genome-wide screening did not identify Ras and its effectors as central components mediating sunitinib resistance in ccRCC cells.