Since NF-κB signaling pathway is known to regulate the expression of CXCL1 (29, 30), which in turn promotes chemotaxis of MDSCs and TAMs through CXCR2 receptor (31–33), our data together suggest that SQLE likely affects cancer immunity through metabolic elimination of squalene, leading to activation p65/NF-κB signaling pathway and high expression of CXCL1 to exert its chemotaxis effect on MDSCs and TAMs, which promote the formation of an immunosuppressive tumor microenvironment. The gene discussed is NFKB1; the disease is neoplasm.