While further studies are required to definitively address whether Ctx-induced non-viable cells express the highest levels of AREG/EREG and/or the lowest levels of FGFR3 activity, it is reasonable to suggest that as the AREG/EREG cross-suppressive mechanism allows for a rapid cancer cell camouflage from Ctx molecular functioning, cross-suppression of AREG/EREG may facilitate survival in Ctx-treated tumour cells, likely promoting their own resistance if the Ctx-induced EGFR blockade persists. The gene discussed is EREG; the disease is cancer.