Our observations of increased induction of CXCL10 and CXCL11 in the case of anti-TIGIT and anti-PD-1 combination treatment allows us to formulate a hypothesis where an anti-TIGIT antibody with FcγR binding-competent Fc moiety enhances anti-tumor activity through FcγR engagement of monocytes triggering the paracrine CXCL9, –10, –11/CXCR3 pathway leading to increased migration and activation of immune cells in the TME. The gene discussed is CXCR3; the disease is neoplasm.