SOST and Dravet syndrome: Sclerostin, the product of the SOST gene, produced mainly by osteocytes, is a potent negative regulator of bone formation via inhibition of the Wnt signaling pathway.17 Although a promising treatment candidate that increases bone mineral density and bone formation with decreased bone resorption in postmenopausal women with low bone mass,18 the potential utility of antisclerostin therapy to increase bone mass in challenging patient populations such as DS is unknown.