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Functionally, GAS6 overexpression enhanced cancer cell survival, whereas a new anti\u2010GAS6 antibody delayed tumor relapses in xenograft models. Similarly, ablation of MERTK sensitized lung cancer cells to osimertinib, revealing a bypass crosstalk between EGFR and MERTK, likely taking place within caveolae. An anti\u2010MERTK antibody was generated, and a bispecific antibody, Bis\u2010EM, targeting both EGFR and MERTK, was designed. Bis\u2010EM promoted the degradation of both receptors and displayed the capacity to promote immune\u2010mediated cell killing. In combination with TKIs, concurrent antibody\u2010mediated inhibition of MERTK and EGFR suppressed the growth of TKI\u2010resistant spheroids. Co\u2010treatment with Bis\u2010EM and TKIs delayed tumor relapses in an Fc\u2010dependent manner across patient\u2010derived xenografts harboring clinically challenging EGFR exon 20 insertions and other mutations. Collectively, these findings identify the GAS6\u2013MERTK axis as an important driver of drug resistance and provide a strong rationale for the clinical development of Bis\u2010EM.<\/jats:p>","DOI":"10.1002\/advs.78290","type":"journal-article","created":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T04:11:07Z","timestamp":1792037467000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Fc\u2010Dependent Targeting of the GAS6\u2013MERTK Axis With Monoclonal and Bispecific Antibodies Overcomes Drug Resistance Across EGFR Mutations in Exons 19, 20, and 21"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7595-1359","authenticated-orcid":false,"given":"Suvendu","family":"Giri","sequence":"first","affiliation":[{"name":"Department of Immunology and Regenerative Biology Weizmann Institute of Science  Rehovot 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