These results raise a few interesting questions regarding SHMT nuclear function: it is not known if the scaffolding role of SHMT1 can be untied from its enzymatic activity; would K39 SHMT1 mutants, unable to undergo SUMOylation and translocate to the nucleus, lead to more severe DNA replication and folate-deficiency associated phenotypes than catalytically dead SHMT1 mutants? The gene discussed is SHMT1; the disease is hyperinsulinemic hypoglycemia, familial, 4.