Nevertheless, in vitro studies using siRNA-mediated knock-down of the EGFR indicate that the proliferation of NSCLC cells expressing wild-type EGFR and bearing mutated KRas is still dependent to some extent on the EGFR [9], [10], [11], [12] suggesting that EGFR-TKI resistant cells are not totally independent of the EGFR and that, therefore, targeting the EGFR by means other than TKIs might lead to reduced proliferation even in EGFR-TKI resistant cells. This evidence concerns the gene EGFR and non-small cell lung carcinoma.