SEC23A and hyperinsulinemic hypoglycemia, familial, 4: Consistent with this hypothesis, murine Sec23a gene expression has been shown to be maintained throughout erythropoiesis, in contrast to human SEC23A expression, which declines rapidly upon induction of terminal erythroid differentiation (74), potentially explaining the absence of a red blood cell phenotype in mice with hematopoietic deficiency of SEC23B (71).