Moreover, inactivation of TP53 function in EGFRM+ NSCLC may also occur post-transcriptionally via another frequent primary co-alteration, i.e., de novo amplification of the MDM2 oncogene, which results in inhibition of the p53 protein [38] and is associated with worse PFS during TKI-treatment with osimertinib [124]. This evidence concerns the gene TP53 and non-small cell lung carcinoma.