In fact, though, these drugs dramatically benefit only a small percentage of cancer patients, based on the alterations concerning EGFR itself (e.g., specific mutations targeted by small molecule tyrosine kinase inhibitors [TKIs]) or molecules in the EGFR effector pathways (for example, KRAS [official gene name: v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog; aliases: KRAS2, RASK2] mutations hampering therapeutic EGFR antibodies and possibly TKIs as well). This evidence concerns the gene EGFR and cancer.