To explore the clinical value of tumor suppressor MrgprF, we discovered that AMG 706, the originally ATP-competitive inhibitor of VEGFR1, VEGFR2, VEGFR3, platelet-derived growth factor (PDGF) receptor (PDGFR) and stem cell factor (SCF) receptor (Kit), well-known receptors critical for promoting cancer cell survival and growth,39 increased MrgprF expression via reducing DNMT3A and DNMT3B expression, and the detail regulatory mechanism should be further characterized in the future (Fig. 6g). Here, FLT1 is linked to neoplasm.