The role for the NF-κB signaling pathway in promoting skin SCCs has also been demonstrated [24,25]: it was shown that NF-κB inhibition in keratinocytes prevented tumor development by acting both during the initiation and promotion phases of skin carcinogenesis; i.e., mice with keratinocyte-restricted p65 deficiency were resistant to 7,12-dimethylbenzanthracene/12-O-tetradecanoylphorbol-13-acetate (DMBA/TPA)-induced skin carcinogenesis, supporting the tumor-promoting role of epidermal p65 through NF-κB activation [26]. Here, NFKB1 is linked to neoplasm.