It is caused by mutations in the gene PVRL1 (11q23-q24) which encodes nectin-1, the principal receptor used by alpha-herpesviruses to mediate entry into human cells. Although the mechanism underlying the physiopathology of this syndrome is still unknown, it has been proposed that nectin-1 is a cell-cell adhesion molecule that is preferentially expressed in keratinocytes and that mutations in PVRL1 may abrogate NAP (nectin, afadin, ponsin)-dependent cell-cell adhesion.It is thought that the genetic transmission is autosomal recessive gene transmission.8
Rosselli–Gulienetti syndrome
Naegeli–Franceschetti–Jadassohn syndrome
Gómez–López-Hernández syndrome
Muir–Torre syndrome
Galloway Mowat syndrome
Sanjad-Sakati syndrome
Fraser syndrome
Townes–Brocks syndrome