Studies investigating therapeutically-induced immune responses in the MC38 model have shown that these tumours evade anti-tumour immunity through a variety of different mechanisms, including the recruitment of regulatory CD4+ T cells (TREG) (19), the expression of inhibitory ligands such as PD-L1 by tumour and myeloid cells (15), and by inducing the dysfunction of infiltrating CD8+ T cells (32, 33). The gene discussed is CD274; the disease is neoplasm.