Our earlier study also found that in a 7,12‐dimethylbenz[a]anthracene/phorbol ester 12‐O‐tetradecanoylphorbol 13‐acetate (DMBA/TPA)‐induced skin carcinogenesis model, transgenic SAG expression inhibits the early‐stage tumor progression by promoting c‐Jun degradation to inhibit AP‐1, and accelerates the late‐stage tumor growth by promoting IκBα degradation to activate NF‐κB and inhibit apoptosis.1 The gene discussed is SAG; the disease is neoplasm.