Egfr, short for Epidermal Growth Factor Receptor, belongs to the ERBB family of tyrosine kinase receptors. Its signaling cascade is crucial in regulating cell proliferation, differentiation, division, survival, and is also involved in cancer development. Activation of Egfr leads to autophosphorylation of receptor tyrosine kinase, initiating downstream signaling pathways related to cellular processes [1,5].

Egfr mutations are the second most common oncogenic driver event in non-small cell lung cancer (NSCLC). Classical activating mutations like exon 19 deletions and the L858R point mutation are strong predictors for a good response to Egfr tyrosine kinase inhibitors (Egfr-TKIs). However, low-frequency mutations in exons 18-25 are associated with poorer responses [2]. In addition, inappropriate activation of Egfr in cancer mainly results from amplification, point mutations, transcriptional upregulation, or ligand overproduction. Moreover, it is increasingly recognized as a biomarker of resistance in tumors due to amplification or secondary mutations under drug pressure [3].

In conclusion, Egfr is essential in regulating epithelial tissue development and homeostasis. Its dysregulation is closely associated with cancer, especially NSCLC. Understanding the role of Egfr through studying its mutations and functions provides insights into targeted cancer therapies, especially the development and resistance of Egfr-TKIs in treating NSCLC [2,3,4,6,7].