(1) In the prostate there are indications that loss of FGFR2-IIIb stimulation by its ligand FGF7 contributes to the switch—indicating that the activated receptor reinforces its own expression [64]; (2) in NBT-II rat bladder carcinoma cells and SVK14 human keratinocytes, exogenous FGF1 or FGF2 induced an FGFR2 IIIb/IIIc switch [65]. Here, FGFR2 is linked to urinary bladder carcinoma.