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Tumor metabolism and epigenetic regulation are two fundamental mechanisms that modulate cancer stemness. Lactylation, a novel post\u2010translational modification, has emerged as a pivotal bridge linking these two processes. Accumulating evidence highlights elevated lactylation as a critical driver of cancer stemness. To elucidate the underlying mechanisms, we systematically evaluate how lactylation orchestrates the cancer stem cell (CSC) landscape across four functional dimensions: self\u2010renewal maintenance, stemness\u2010associated signaling activation, microenvironmental adaptation, and lineage plasticity induction. Furthermore, we summarize the dynamic regulatory network governing this modification, comprising both key enzymes and indirect modulators. Beyond highlighting promising therapeutic targets and preclinical successes, we critically assess the significant challenges hindering clinical translation. 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