Since mice heterozygous for a null mutation of PolB show significantly higher mutation rates in sperm than WT mice [32] and PolB+/C mice develop an autoimmune pathology that resembles systemic lupus erythematosus, a condition that has been suggested to reflect a BER deficiency [33], we rationalized that an effect of the Polβ mutation on expansion might be seen even in heterozygotes. The gene discussed is POLB; the disease is hyperinsulinemic hypoglycemia, familial, 4.