The antitumor response elicited by radiation therapy can be enhanced by unleashing immune resistance mechanisms through the use of immune checkpoint blockers [such as anti-cytotoxic T-lymphocyte-associated protein-4 (anti-CTLA-4) or anti-PD-L1 antibodies], revealing that the modulation of the cross-talk between the biological effects of radiation therapy and the immune system is central for optimal tumor growth inhibition (4). The gene discussed is CTLA4; the disease is neoplasm.