<p>Tumor recurrence often occurs years after initial treatment, driven by dormant tumor cells that evade detection and therapy. These quiescent cells can persist in primary or metastatic niches and later reawaken under favorable microenvironmental conditions, contributing to cancer relapse. Tumor-associated macrophages (TAMs) have emerged as key regulators in orchestrating this proliferation-dormancy switch. Through secretion of cytokines, extracellular vesicles, and direct cellular interactions, macrophages influence tumor cell fate via multiple signaling pathways, including TGF-β, WNT, and HIPPO. These pathways modulate the expression of cell cycle regulators, such as cyclins and cyclin-dependent kinase inhibitors (CKIs), ultimately governing the transition between proliferation and dormancy. This review synthesizes current findings on the roles of macrophages in initiating and maintaining tumor cell dormancy across various solid tumors. We discuss how distinct macrophage subtypes—defined by developmental origin or polarization state—differentially engage with tumor cells to modulate dormancy-associated signaling cascades. Understanding these spatiotemporal interactions between macrophages and tumor cells offers novel opportunities for therapeutic intervention aimed at preventing relapse by targeting the dormant tumor cell niche.</p>