Enzymatic stability and catalytic efficiency of the GALE enzyme could be causative factors in the continuum of GALE deficiency [31], since patients with peripheral GALE deficiency show normal enzyme activity in liver and fibroblasts versus patients with generalized GALE deficiency who show profoundly decreased enzyme activity in other cell types, such as liver and fibroblasts [9, 32]. This evidence concerns the gene GALE and galactose epimerase deficiency.