PTEN and neoplasm: Correlating with this, genetic crosses of Cdkn1b+/- and Cdkn1b-/- mice with mammary (MMTV-neu) [44] and prostate (Nkx3.1and Pten deficient) [45] tumor models also demonstrated a dosage sensitive effects as Cdkn1b+/- crosses increased tumorigenesis, while complete deletion of p27 decreased it.