NIN and Hip dysplasia: Grosch et alidentified homozygous missense mutations in NIN (Ninein) and POLE2 in four members of a Turkish consanguineous family with clinical and radiological features of SEMDJL2 which segregated in the family and was not present in 500 healthy control individuals.3 The proband had short stature (-5.2 SD), bilateral hip dysplasia, short arms and legs, laxity of small and large joints, genua valga, pes cavus, no intellectual disability, and mild facial dysmorphism.