Second, the phenotype of p73-/- mice (generated by deleting the exons encoding the DBD, thus affecting all p73 isoforms) offered no evidence for p73 role in cancer; p73-null mice had neurological (hydrocephalus), pheromonal, reproductive, inflammatory and behavioral defects, but showed no increased susceptibility to spontaneous tumorigenesis, since they die 4-6 weeks after birth [23]. This evidence concerns the gene TP73 and cancer.