Selective FGFR inhibition might prove clinically ineffective as a monotherapy in STS patients despite promising preclinical evidence due to several reasons: FGFRs might be amplified only in a subpopulation of cells, therefore representing a non-driver event; variable addiction to FGFR amplification might be modulated by the expression or mutation of other transducing molecules such as components of the MAPK pathway; and activating alternative oncogenic pathways (in particular VEGFR and PDGFR) that may compensate for FGFR inhibition [97]. Here, PDGFRB is linked to telomere syndrome.