Based on this evidence, and the high levels of HLA-DR, FGL-1, and galectin-3 cognate ligands at tumor site, it is tempting to speculate that systemic LAG-3 blockade might have triggering an immunological cascade leading to the expansion of active immune effectors which would eventually migrate to tumor site to mediate the complete tumor regression observed in our patient, with PD-1 blocker possibly amplifying and prolonging the immunomodulating effect13. The gene discussed is LGALS3; the disease is neoplasm.