GALE deficiency inhibits UDP-glucose regeneration, preventing the formation of glucose-1-phosphate and leading to the accumulation of galactose and galactose-1-phosphate. High galactose-1-phosphate levels have been shown to interfere with phosphoglucomutase,[7] glycogen phosphorylase,[8] UDP-glycopyrophosphorylase,[9] and inositol monophosphatase[10] activity in bacterial models and in vitro, yet in vivo mechanisms toxicity have yet to be confirmed.[3] Regardless, median galactose-1-phosphate levels act as the most accurate predictors of the severity of symptoms associated with Type III galactosemia.[11]