EGFR and non-small cell lung carcinoma: The reason we postulated STAT3 as a potential target of ESB was based on the following points: (i) STAT3 frequently overactivated in NSCLC contributed to cancer progression by regulating major cancer hallmarks, such as cell proliferation, angiogenesis, metastasis, the evasion of immune surveillance, and chemoresistance [25,26,27], (ii) the level of STAT3 phosphorylation was higher in the EGFR TKI-resistant tumors than in the EGFR TKI-naïve or -sensitive tumors [28,29,30], and (iii) previous studies postulated STAT3 as a key mediator of both primary and acquired resistance to EGFR TKIs [31].