SMAD4 and hereditary hemorrhagic telangiectasia: As HHT progresses by the loss of heterozygosity via somatic mutations on the healthy alleles of BMP pathway components in a subset of endothelial cells within a vascular plexus, a model for cell migration that more closely resembles the in vivo situation of HHT would be to look at a mosaic scenario where only a subset of cells are deficient for SMAD4 or Alk1.