The relevance of this observation is not obvious considering that: i) FPR1 is overexpressed in human primary melanoma and associates with aggressive phenotype [35]; iì) In human glioblastoma and neuroblastoma cells, FPR1 promotes cell growth, invasion and production of angiogenic factors [37]; ììì) In glioblastoma, FPR1 exploits the function of EGFR to promote tumor progression by increasing the phosphorylation on Tyr992 in the intracellular tail of EGFR [51]. The gene discussed is FPR1; the disease is neoplasm.