We also found no difference in tumor macrophage M1 (CD86 staining) and M2 (CD163 staining) populations between the control and Pramlintide-treated tumors (Figure S3), suggesting that Pramlintide-induced antitumor activity in this model was via a direct effect on the tumor cells and not mediated by immune cells or an effect on the tumor vascularity. The gene discussed is CD86; the disease is neoplasm.