This notion is further supported by findings from Alameda et al. that expression of a catalytically inactive form of CYLD in a Ha-ras-mutated tumorigenic epidermal cell line (PDVC57) significantly promoted in vitro cell proliferation, migration (with changes to a mesenchymal phenotype), anchorage-independent growth, as well as pronounced in vivo tumor growth and angiogenesis with upregulation of vascular endothelial growth factor-A (VEGF-A) expression [28]. This evidence concerns the gene CYLD and neoplasm.