  In contrast to its cognitive profile, which is, as we have seen, a  subject of debate, the genetic basis of WS is known. It results from  a ≈1.5 Mb deletion encompassing the elastin gene ELN at  chromosome 7q11.23; most cases appear to be due to new mutations. ELN is crucial in synthesizing elastin, a protein which holds cells  together in the elastic fibers found in connective tissues throughout the body and in especially high concentrations in cartilege,  ligaments and arterial walls. Failure to synthesize this protein  disrupts development in numerous ways, from the first trimester  onwards, and gives rise through processes that are not well  understood to the raft of symptoms associated with the syndrome.  (Morris and Mervis 2000; Mervis et al. 2000.)