Furthermore, a small proportion of patients with RET fusion-positive NSCLC were also found to have other driver alterations, such as EGFR and KRAS. However, acquired RET fusions have been described as a mechanism of resistance to targeted therapies, such as EGFR inhibitors and without complete clinical annotation, it is difficult to determine if these were de novo alterations or acquired in the setting of targeted therapy. This evidence concerns the gene KRAS and non-small cell lung carcinoma.