However, they do play an import role in mammalian cells as Dph1 null mice display multiple developmental defects that parallel Miller-Dieker syndrome (MDS) (Yu et al. 2014), associated with deletions on chromosome 17p13.3, Dph3 null mice are embryonically lethal (Liu et al. 2006) and Dnajc24 (Dph4) null mice almost always die before birth with the few that do survive showing severe developmental defects reminiscent of Dph1 null mice (Webb et al. 2008). Here, DNAJC24 is linked to Miller-Dieker lissencephaly syndrome.