In the tumor microenvironment, 20-HETE modulates immune responses; Chen et al. [39] demonstrated that 20-HETE activates tumor-associated fibroblasts through the GPR75/STAT3/c-Jun signaling pathway, thereby promoting immune evasion and enhancing the invasiveness of non-small-cell lung cancer (NSCLC) cells. The gene discussed is JUN; the disease is neoplasm.