Since the first patient with this T−B+NK+ SCID was identified in 2009,1 a series of patients with CORO1A protein deficiency have been reported and the disease’s spectrum has been expanded to include a milder phenotype that is caused by hypomorphic CORO1A mutations and leads to T-cell lymphopenia of variable severity, profound defects of naive T-cells, seemingly preserved B- and natural killer (NK) cell compartments, recurrent viral infections, and EBV-associated B-cell lymphoproliferation.2, 3, 4, 5, 6, 7, 8, 9. This evidence concerns the gene CORO1A and hyperinsulinemic hypoglycemia, familial, 4.