Two lines of evidence support this claim: first, IL27-treated CD11b−/− mice are 4 times less likely to develop papillomas and promote angiogenesis in the pre-malignant skin when compared to control, and second, ETAR is mainly upregulated in CD11b-positive cells and ETAR depletion via a chemical inhibitor significantly delayed IL27-dependent papilloma development in the K15-driven oncogenic KRAS model. The gene discussed is EDNRA; the disease is papilloma.