 Pancreatic cancer is characterized by an extensive fibro-inflammatory stroma rich in macrophages which suppresses the immune system and impairs the effectiveness of immunotherapies. Macrophages expressing the enzyme arginase 1, ARG1, are particularly abundant in pancreatic cancer, and their activity reduces the availability of arginine and essential amino acid for T-cell activation and proliferation. We have shown that targeting ARG1 in macrophages can delay the development of pancreatic cancer, increase CD8 plus T-cell infiltration, and enhance the efficacy of immunotherapeutics. Furthermore, our findings suggest that compensatory mechanisms exist to counteract the effects of ARG1 inhibition, such as increased ARG1 expression in epithelial cells and increased ARG2 expression in macrophages. These results highlight the importance of understanding the underlying mechanisms of immune suppression in pancreatic cancer and provide evidence for the potential use of ARG1 inhibitors in combination with immunotherapies. This article was authored by Rosa E. Menjivo, Tereb C. Nwosu, Wantingdu, and others. We are article.tv, links in the description below.