Whilst the phenotypes in the TGF-β deficient mutant mice are dramatic and restricted to specific compartments [58-60], it is clear that multiple tiers of control are present in the human disease- LOI at chromosome 11 leading to raised levels of TERT, IGF2, etc. The heterozygous TGF-β deficient mutants develop cancers spontaneously on a C57BL/6 background and in this regard the heterozygotes resemble sporadic cancer formation in humans [61-63]. Here, TERT is linked to cancer.