The current evidence may suggest that a galectin-1 inhibitor in combination with existing therapies, such as chemotherapeutic agents and/or checkpoint inhibitors, or even as a monotherapy, may reduce the pro-tumour effects of IL-17A, IL-6, IFNγ and TNFα and turn a “cold”, immunosuppressed TME into a “hot”, inflamed, cytotoxic T cell-rich TME, resulting in increased tumour cell killing and enhanced cancer prognosis and survival. This evidence concerns the gene LGALS1 and neoplasm.