Noteworthy are VEGF, constitutively highly expressed as compared to rats [7]; p53 that harbors substitutions in the DNA-binding site, identical to the most common p53 mutations in tumors; however, in Spalax it renders a bias against apoptosis but favors cell cycle arrest/DNA repair both in vitro and in vivo[8]; and a unique Spalax heparanase splice variant that was shown to decrease tumor size in mice by a factor of 7 and reduce metastatic activity compared to native mice heparanase [9]. The gene discussed is HPSE; the disease is neoplasm.