Therefore, our objectives were: 1) to determine if UTMC enhances eATP with CD39 inhibition, 2) to investigate whether enhanced ATP with CD39 inhibition induces vascular inflammation, 3) to assess if enhanced ATP causes cancer cell death, 4) to assess if CD39 inhibition can enhance UTMC + ICB efficacy, and 5) to determine if the immune cell responses in TME are shifted toward an inflamed TME. The gene discussed is ENTPD1; the disease is cancer.