We have recently reported that the receptor tyrosine kinase, c-Met (mesenchymal-epithelial transition factor), which is over-expressed in renal cancer, promotes the survival of renal tumor cells through the regulation of the anti-oxidant cytoprotective molecule heme oxygenase-1 (HO-1); c-Met also modulates the expression of the negative co-stimulatory molecule, PD-L1 (Programmed Death-Ligand 1), involved in immune escape of renal cancer cells [14]. This evidence concerns the gene HMOX1 and renal carcinoma.