The observation that in several non-endocrine human tumors somatic biallelic inactivation of CDKN1B is exceedingly rare led to the hypothesis that p27 is a dose-dependent (haploinsufficient) tumor suppressor (Philipp-Staheli et al., 2001), as formally demonstrated in mice (Fero et al., 1998). This evidence concerns the gene CDKN1B and neoplasm.