Interestingly, while syndromic and nonsyndromic CS differ in extracraniofacial presentation and in the pattern and degree of suture involvement, the histomorphometric phenotype at the level of the pathologic closed/closing suture is virtually indistinguishable.(37) This implies that even widely disparate regulatory factors such as fibroblast growth factor receptors (FGFRs) 1, 2, and 4 and Twist causing distinctly different CS syndromes nonetheless may converge mechanistically at the level of the calvaria to affect suture fusion. The gene discussed is TWIST1; the disease is Cowden syndrome 1.