Thus, considering the correlation between therapy resistance and TREG percentages in our cultures, the inactivity of anti-TIM-3 antibodies against galectin-9 interactions, and the growing evidence of galectin-9 role in tumor immune escape [48, 49], we moved to explore galectin-9 as an interesting target to improve rituximab-induced depletion. The gene discussed is HAVCR2; the disease is neoplasm.