Resistance might also be mediated by an inhibitory effect of erlotinib on UGT1A1-mediated glucuronidation within the tumour cells.38 For example, several tyrosine kinase inhibitors have been shown to inhibit UGTs, leading to drug–drug interactions that may influence response to other anti-cancer drugs by altering the elimination of co-administered drugs.39 The potent inhibition of UGTs by tyrosine kinase inhibitors could also potentially have a significant clinical effect on the metabolism of endogenous oncogenic substrates involved in cancer-cell progression. The gene discussed is UGT1A1; the disease is cancer.