Collectively, these studies suggest that high mutation burden as a result of genomic instability and the consequent increased in tumour surface neoantigens leads to an increased in tumour-infiltrating immune cells and ultimately the compensatory up-regulation of the PD-1/PD-L1 pathway as a mechanism of inhibiting T-cell activation at tumour sites [17, 18]. The gene discussed is CD274; the disease is neoplasm.