Our previous studies of skin carcinogenesis in nude mice showed that the lack of the catalytic function of CYLD increased the aggressiveness of cutaneous SCCs [10,30]; i.e., we found that the expression of the mutant CYLDC/S, which acts as a dominant negative by inhibiting the deubiquitination function of the endogenous CYLD, enhanced tumor cell proliferation, survival, and tumor angiogenesis (the latter considered a prominent feature of skin tumor progression) in both mouse and human skin SCCs [10,30,42]. Here, CYLD is linked to neoplasm.