Tumor microenvironment (TME) not only promotes the early formation and distant metastasis of tumors but also changes constantly with the progress of tumors. Cancer stem cells (CSCs) are self-renewing cells that facilitate tumor initiation, promote metastasis, and enhance cancer therapy resistance. The crosstalk between CSCs with cancer cells and other non‐CSCs occurs in cancers, which is possible under the control of signals from CSCs and TME, including CSCs niche. As an important immune cell in CSCs niche, tumor-associated macrophages (TAMs) are among the most influential cells for promoting CSCs survival, and self-renewal. TAMs can activate IL-6 /STAT3, TGF-β, Wnt/β-catenin, and other signaling pathways by secreting a series of cytokines to promote survival, self-renewal, and resistance to chemotherapy of CSCs. At the same time, CSCs also play an important role in promoting the recruitment of macrophages and inducing their transformation into M2 TAMs to promote tumor progression. CSCs recruit macrophages into TME through various secretory factors such as POSTN, MIF, CCL2, M-CSF, IL-6, IL-1β, TNF-α, etc, and then polarize to the M2 phenotype under the action of PGE2, WISP, IL-10, GM-CSF, MIC-1, and other chemokines and cytokines, shaping immunosuppressive and tumor-promoting TME. Therefore, the interaction between TAMs and CSCs plays an important role in promoting tumor growth, metastasis, and chemoresistance. This paper reviews the research progress on the interaction between CSCs and TAMs in TME and the potential target in the interaction of CSCs and TAMs for novel cancer therapy. These emerging insights provide a roadmap for the development of novel anti-cancer therapeutic strategies that disrupt this dynamic circuit in specific tumor types.