Across both genotypes, tumour-resident CD103+ DCs expressed 1.5–3-fold higher levels of both co-stimulatory (CD80/B7-1, CD86/B7-2) and –inhibitory (PD-L1/B7-H1, PD-L2/B7-DC) surface molecules as compared to CD103− DCs (Fig. 3c and Supplementary Fig. 4a). This evidence concerns the gene CD86 and neoplasm.