While additional studies are required to define the specific mechanisms by which ERBB receptors contribute to signalling in FGFR3-fusion driven bladder cancers following FGFR inhibition, our findings in the SW780 and RT4 cell lines adds to the previous findings in RT-112 cells to demonstrate compensatory activation of ERBB3-driven signalling as a consistent mechanism of rapid adaptive resistance to FGFR inhibitors in these tumours. This evidence concerns the gene FGFR3 and neoplasm.