More than 50% of these proline-directed phosphosites were upregulated in adenocarcinoma A549 (harboring the KRASG12D mutation) and H322 (KRAS amplification) cells, but not in LCC H1299 (NRASQ61K) cells (Figure 3E and Table 1), in agreement with previous reports that oncogenic KRAS, but not oncogenic NRAS, is effective in stimulating downstream MAPK signaling 30,31]. This evidence concerns the gene NRAS and adenocarcinoma.