MLH1 and cranioectodermal dysplasia: Indeed, although the casual co‐occurrence of CeD and SBA cannot be excluded in a few CeD‐SBA cases, the distinctive molecular features of CeD‐SBA, including the significantly higher rates of dMMR/MSI, MLH1 and APC methylation, and nuclear expression of β‐catenin compared with sporadic cases, support the role of CeD in the pathogenesis of CeD‐SBAs [26, 66, 67].