Considering that the atypical keratinocytes in SCC and AK express CYP1A1, AhR ligands stimulate NHKCs to increase the production of CYP1A1 as well as proinflammatory cytokines (18), and since IL-17 could drive the tumor progression through TRAF-ERK5 pathways in cSCC (16), we next examined the immunomodulatory effects of FICZ and DMBA on NHKCs, focusing on the expression of CYP1A1, CCL20, p19, p40, IL-36α, IL-36β, and IL-36γ mRNA at 4 h after stimulation in vitro. The gene discussed is IL36B; the disease is neoplasm.