However, when SQLE expression is elevated in cancer such as in pancreatic ductal adenocarcinoma, its high enzyme activity could then promote the metabolic conversion of squalene to oxidosqualene, leading to a significant decrease of squalene and thus less inhibition on NF-κB signaling pathway, which in turn promotes CXCL1 expression to recruit more MDSCs and TAMs to the tumor tissues, and thus creating an immunosuppressive and pro-tumor microenvironment. The gene discussed is CXCL1; the disease is neoplasm.