Cbl is likely to be, at least in part, functionally deficient in sepsis, as indexed by the down-regulation of the Cbl receptors, megalin and cubilin, in the kidneys of endotoxaemic mice [65], the kidney being known, as a Cbl homeostatic regulator, to reduce its Cbl uptake in states of Cbl deficiency [66]. The gene discussed is CBL; the disease is hyperinsulinemic hypoglycemia, familial, 4.