In summary, we find that the synergy between RT and anti‐PD‐L1 observed in our experimental tumor growth curves can be explained by a model where (i) RT induces a large population of tumor cells to become susceptible to immune cell killing and (ii) anti‐PD‐L1 increases the recruitment and killing ability of CD8 T cells and, importantly, prevents the establishment of suppressive microenvironment factors (Appendix Fig S11A and G). The gene discussed is CD8A; the disease is neoplasm.