It has been well established that TAMCs can stimulate the proliferation of CAFs through secreting IL‐13 and tryptase.[36] Building upon this foundation, our study identified and validated a novel finding: TAMC activation after AG neoadjuvant therapy induced CAFs to shift the phenotype from myCAFs, which are involved in ECM remodeling and then promoting tumor invasion, metastasis, and therapeutic resistance, to the iCAFs, which exert pro‐inflammatory polarization and interfere with the TME by secreting inflammatory mediators. This evidence concerns the gene IL13 and neoplasm.