Based on next-generation sequencing (NGS) of circulating tumor DNA (ctDNA) and tumor samples from patients who experience disease progression on osimertinib, identified mechanisms of resistance can be broadly divided into EGFR-dependent mechanisms (alterations preventing osimertinib inhibition of EGFR) and EGFR-independent mechanisms (activation of alternate signaling pathways or reprogramming, such as epithelial–mesenchymal transition and histologic transformations)12,13. This evidence concerns the gene EGFR and neoplasm.