Therefore, we sought to establish the following: (a) whether cross-regulation mechanisms can explain the impact of AREG/EREG on Ctx efficacy; (b) whether the loss of AREG or EREG is sufficient to fully establish tumour resistance to Ctx; (c) whether the downregulation of AREG/EREG expression is indispensable for the Ctx mechanism of action; and/or (d) whether kinase-switching phenomena might contribute to bypass loss of EGFR-ligand signalling caused by Ctx. This evidence concerns the gene CYP27A1 and neoplasm.