Studies from other groups indicate that CBS-mediated H2S overproduction impairs mitochondrial bioenergetics in DS patient-derived fibroblasts and disrupts neurobehavioral function in a DS mouse model, and that these deficits were rescued after the pharmacological inhibition of CBS with aminoxyacetic acid (AOAA) or gene silencing with anti-CBS siRNA [10,11,12]. This evidence concerns the gene CBS and Dravet syndrome.