Contact of IL30-overexpressing PC cells with the endothelium further increases their expression of growth factors and proinflammatory mediators, including VEGFA, CCL28, CCL4, CCL5, CCR2, CCR7, CXCR4, IL10, IL13, IL17A and promotes mechanisms of immune privilege by upregulating cancer cell expression of FASLG, IDO1, KITLG [78], apoptosis inducing ligand TNFSF10/TRAIL [79] and PDCD1/PD-1, which is involved in tumor initiation and progression [80]. This evidence concerns the gene FASLG and cancer.