Besides promising and effective, the treatment with third generation EGFR TKIs showed that resistance can still reemerge, due to further modifications in the receptor, mainly C797S mutation but also alternative pathway activation, such as those involving HER2 and MET amplification or G12S KRAS mutation, other than histologic transformation in the case of NSCLC, making them phenotypically transform into small cell lung cancer (SCLC) [13, 14]. Here, KRAS is linked to non-small cell lung carcinoma.