As a result of our study and in conjunction with recent reports describing that the overexpression of Survivin favors the progression from chemically induced papilloma to squamous cell carcinoma in K14-Survivin transgenic mice [57] and initiates hematological malignancies in GATA1-Sur transgenic mice after a single intraperitoneal injection of tumor promoting N-ethyl-nitrosourea [58], it appears also conceivable that besides Survivin’s IAP function deregulations in the mitotic function of Survivin favor the development of aneuploid cells. This evidence concerns the gene KRT14 and neoplasm.