On the one hand, since GPC1 is known to act as a co-receptor by sequestering the FGFs on the cell surface, stabilizing the FGF ligand-receptor interaction and subsequently improving the efficiency of FGF-activated FGFR1 signaling pathways in tumor cells [5, 6, 42], it is conceivable that inhibition of GPC1 activity with the anti-GPC1 mAb is able to impede the activation of signaling pathways downstream of FGFR1. This evidence concerns the gene FGFR1 and neoplasm.