We have previously demonstrated that in conditions of relative RTK excess, a PRM sequence incorporated within the C-terminal tail of FGFR2 induces activation of intracellular effectors through SH3 domain-mediated interactions that occur in the absence of tyrosine kinase upregulation, and which associate with disease outcomes in a number of cancers [[18], [19], [20]]. Here, FGFR2 is linked to cancer.