For example, capsaicin was shown to be co-carcinogenic in rodent skin [70] and the TRPV1 antagonist AMG9810 was shown to act as a tumor promoter [71] However, in the former study, the effects of capsaicin turned out to be mediated by EGFR signaling, independent of TRPV1, while in the latter study, the TRPV1 dependence of the AMG9810 effects, which also somehow involved EGFR signaling, was not directly addressed. The gene discussed is TRPV1; the disease is neoplasm.