Regenerative therapy in diabetes with the capacity to reconstitute a functional β-cell mass sufficient for glycemic control holds the promise to effectively prevent the development of devastating late complications due to the unique ability of the β-cell to sense and regulate blood-glucose levels. An ability that cannot be mimicked by insulin replacement therapy or any other means of current treatment regiments for very large patient populations. Recently, Douglas A. Melton’s group from Harvard University reported the identification of a circulating protein secreted from the liver under insulin resistant states which is sufficient to dramatically and specifically increase the replication rate of β-cells in the mouse resulting in an increased functional β-cell mass over time. They re-named the factor betatrophin and described a number of exciting features of this molecule which suggested that it could be a potential candidate for development as a regenerative medicine in diabetes.(1) The official name of the gene encoding mouse betatrophin is Gm6484, but it has been annotated a number of times under different names: EG624219(2)(,)(3), RIFL(4), Lipasin(5) and ANGPTL8.(6) The official human gene name is C19orf80, but it has also been annotated as TD26(7), LOC55908(8), as well as RIFL, Lipasin, ANGPTL8 and betatrophin.