MBL-depleted mice show smaller ischemic lesions and fewer deficits after ischemia than their wild-type counterparts,1,2 and these data are paralleled in humans.3 Genetic variants cause MBL deficiency in ~ 20% of the general population,4–7 and stroke patients with MBL deficiency have smaller infarctions and better outcomes than those without,1,8 supporting the hypothesis of a key role of MBL in human stroke pathophysiology. Here, MBL2 is linked to hyperinsulinemic hypoglycemia, familial, 4.