Many heterozygous family members of homozygous protein C-deficient infants are not affected clinically.[10] The treatment of patients with protein C deficiency depends on the risk of thromboembolism, low level of protein C cannot be used as indicator of anticoagulation therapy.[2] Among the healthy population, approximately 0.2% to 0.5% have low protein C levels, and there is no overt clinical thrombotic problem.[11] Oral anticoagulation with a coumarin derivative or heparin remains the fundamental treatment strategies for heterozygous protein C deficiency. The gene discussed is PROS1; the disease is hyperinsulinemic hypoglycemia, familial, 4.