Based on our research and that of other scholars, [67,68], we hypothesize that overexpression of TIAM2 may mediate osimertinib resistance by activating the PI3K/Akt/mTOR signaling pathway to induce M2-like TAM polarization, and thus there is a potential role for TIAM2 in tumor immunotherapy and targeted therapy with osimertinib. Here, AKT1 is linked to neoplasm.