Notably, the treatment also resulted in decreased expression of the mannose receptor Mrc1 (also known as CD206), which is linked to alternative activation of macrophages, and Trem2, a membrane protein associated with tumor promotion and considered a candidate therapeutic target.[2] Furthermore, CANDI460 treatment triggered the upregulation of several inflammatory genes, including Cxcl9 and interleukin Il12a, which are key players in promoting adaptive antitumor immunity[1, 31] (Figure 3G; Figure S8, Supporting Information). This evidence concerns the gene CXCL9 and neoplasm.