KRAS and neoplasm: If AREG/EREG expression is sufficient and necessary to allow for the function of Ctx against EGFR-positive wt KRAS tumour cells, then we may hypothesise that chronic exposure to Ctx will negatively select for initially dominant AREG/EREG-positive (Ctx-sensitive) cells and promote the selection of Ctx-resistant tumour sub-populations exhibiting a downregulated AREG/EREG-driven EGFR signalling cascade and, therefore, Ctx-unresponsive FGFR3-stimulated signalling through the ERK pathway.