Activation of MAPK and Akt are mainstay events in skin carcinogenesis induced by DMBA/PMA.20, 21 Furthermore, MAPKs‐ERK1/2 and p38 are known to operate upstream to β‐catenin in skin cancer.22, 23 Immunoblot analysis of total protein isolated from the dorsal skin of animals revealed that tryptanthrin could accomplish remarkable attenuation of DMBA/PMA‐induced activation of MAP kinases, especially ERK1/2 (Figure 4A, Figure S4A). The gene discussed is AKT1; the disease is skin neoplasm.