In this scenario, the discovery that Arg1, an enzyme contributing to an immunosuppressive microenvironment in many cancers [41], can mediate the tolerogenic signaling triggered upon TLR3/TLR7 stimulation could open new avenues of research to find innovative immunostimulatory drugs inhibiting Arg 1 for improving antitumor immunity in cancer immunotherapy [41]. The gene discussed is TLR3; the disease is cancer.