Thereby, we found that all the investigated cell lines in which the presence of the Spry4 variant identified in Kallmann syndrome inhibited RTK-mediated processes more potently (U2OS, WI38, DMS114) also showed increased protein levels of FGFR1 compared to CRL2868, where no difference in the activity of both variants was observed (Figure 7). This evidence concerns the gene FGFR1 and Kallmann syndrome.