Tumor-associated macrophages (TAMs) are abundant in the tumor microenvironment and play a pro-tumoral role by promoting angiogenesis, tumor cell invasion, and metastasis. They also suppress immune responses by inhibiting natural killer and T cell activity. Therapeutic strategies targeting TAMs, such as inhibiting CSF1 signaling, have shown promise in preclinical models and early clinical trials. TAMs originate from both bone marrow and yolk sac progenitors, with their function influenced by local signals and cytokines. They can be polarized into pro-tumoral or anti-tumoral phenotypes depending on the tumor microenvironment. TAMs contribute to tumor progression by promoting angiogenesis, tumor cell extravasation, and immunosuppression. They also express inhibitory receptors that suppress T cell activation, including HLA-G, PD-1, and CTLA-4. Targeting TAMs through CSF1 inhibition or re-polarization to anti-tumoral states is a promising approach in cancer therapy. Recent studies suggest that TAMs can be targeted to enhance immune responses and improve therapeutic outcomes. The complex roles of TAMs in cancer highlight the need for targeted therapies that specifically address their pro-tumoral functions while preserving anti-tumoral activities.Tumor-associated macrophages (TAMs) are abundant in the tumor microenvironment and play a pro-tumoral role by promoting angiogenesis, tumor cell invasion, and metastasis. They also suppress immune responses by inhibiting natural killer and T cell activity. Therapeutic strategies targeting TAMs, such as inhibiting CSF1 signaling, have shown promise in preclinical models and early clinical trials. TAMs originate from both bone marrow and yolk sac progenitors, with their function influenced by local signals and cytokines. They can be polarized into pro-tumoral or anti-tumoral phenotypes depending on the tumor microenvironment. TAMs contribute to tumor progression by promoting angiogenesis, tumor cell extravasation, and immunosuppression. They also express inhibitory receptors that suppress T cell activation, including HLA-G, PD-1, and CTLA-4. Targeting TAMs through CSF1 inhibition or re-polarization to anti-tumoral states is a promising approach in cancer therapy. Recent studies suggest that TAMs can be targeted to enhance immune responses and improve therapeutic outcomes. The complex roles of TAMs in cancer highlight the need for targeted therapies that specifically address their pro-tumoral functions while preserving anti-tumoral activities.