Histone lactylation (Kla) has recently been recognized as an important epigenetic modification in colorectal cancer (CRC). It is increasingly regarded as a key point of interaction among metabolic reprogramming, gene regulation, and immune microenvironment remodeling. In CRC, enhanced glycolysis leads to marked lactate accumulation in tumor cells and the surrounding microenvironment. Lactate is therefore more than an end product of metabolism. It can drive Kla formation, alter chromatin accessibility, and activate transcriptional programs related to proliferation, invasion, stemness, and immune escape. Kla also affects the immune system at several levels. It can promote M2 polarization of tumor-associated macrophages (TAM), support the homeostasis of regulatory T cells (Treg), induce CD8? T-cell exhaustion, and weaken antigen presentation, thereby forming a persistent immunosuppressive tumor microenvironment (TME). Recent studies further show that Kla forms a relatively stable interactive loop among lactate metabolism, epigenetic regulation, and immune response. This gives Kla both biological importance and potential clinical value in CRC, including possible use in risk stratification, metabolic and epigenetic targeting, and prediction of immunotherapy response. Some issues remain unresolved, especially the identification of the relevant enzymatic system, the standardization of detection methods, and validation in clinical settings. Even so, Kla provides a new perspective for understanding the complex regulatory network of CRC and offers a basis for future combined strategies targeting metabolism, epigenetics, and immunity.