When focusing on the anti-PD1/PDL1 combination with radiotherapy, Dovedi and colleagues suggested that upregulation of anti-PD1 occurs rapidly after radiotherapy and that the mechanism responsible for PD-L1 upregulation in tumor cells involved the production of IFN-y by tumor-infiltrating CD8+ T-cells; therefore, acquired resistance to radiotherapy can be avoided by concurrent administration of PD-L1 with radiotherapy [23,24]. The gene discussed is CD8A; the disease is neoplasm.