FGFR4 SNVs are notable for their prevalence in rhabdomyosarcoma, occurring in 7–8% of cases.24 Specifically, V550E, a gatekeeper mutation, and N535K both contribute to autophosphorylation and constitutive activation of the kinase.25 In a transcriptome screen of cancer cell lines, an FGFR4 Y367C mutation was identified in the human breast cancer cell line, MDA-MB453.26 In vitro characterisation of this mutation showed that it promotes spontaneous dimerisation, resulting in constitutive receptor activation in a ligand-independent manner.27 This evidence concerns the gene FGFR4 and rhabdomyosarcoma.