The proposed pathogenic mechanisms include ovarian damage due to elevated Gal-1-P and galactitol; UDP-Gal deficiency causing aberrant glycosylation of glycoconjugates involved in ovarian function; increased apoptosis of maturing follicles, with accelerated follicle atresia; and possible abnormalities of the immune system, such as unrecognized auto-ovarian antibodies (Forges et al. 2006; Lai et al. 2003b; Liu et al. 2000; Rubio-Gozalbo et al. 2010). The gene discussed is GAL; the disease is hyperinsulinemic hypoglycemia, familial, 4.