Metabolic reprogramming, coupled with PD‐L1 deletion, elevated levels of IL‐6, and extensive infiltration of tumor‐associated macrophages results in a cold immune phenotype in Osimertinib‐resistant models, which complicates the efficacy of immunotherapy.[26, 36, 37, 38, 39] Interestingly, our results reveal that 10e not only promotes the activation of cytotoxic killer immune cells in this tumor microenvironment but also reverses the infiltration proportion of M2/M1‐type macrophages. Here, IL6 is linked to neoplasm.