Nevertheless, depletion of CD8 T-cells from mice bearing PDL1-deficient tumours completely abrogated tumour regressions (Fig. 2j), indicating that despite qualitative changes to the immune and stromal environment, the increased T-effector phenotype remained the main driver behind tumour rejections and interference with the PD-L1/PD-1 pathway. The gene discussed is CD274; the disease is neoplasm.