An identical homozygous missense variant in EIF3F, identified through a large-scale genome-wide sequencing approach, was reported as causative in nine individuals with a neurodevelopmental disorder, characterized by variable intellectual disability, epilepsy, behavioral problems and sensorineural hearing-loss. To delineate and expand the phenotypic and molecular spectrum of EIF3F-related neurodevelopmental disorder, we examined 21 affected individuals, homozygous (20/21) or compound heterozygous (1/21) for c.694T>G/ p.(Phe232Val) in EIF3F. Haplotype analyses in 12 families suggested that c.694T>G/ p.(Phe232Val) was a founder variant. All affected individuals had developmental delays including delayed speech development. About half of the affected individuals had behavioral problems, altered muscular tone, hearing loss, and short stature. Moreover, this study suggests that microcephaly, reduced sensitivity to pain, cleft lip/palate, gastrointestinal symptoms and ophthalmological symptoms are part of the phenotypic spectrum. Minor dysmorphic features were observed, although neither the individuals’ facial nor general appearance were obviously distinctive. Symptoms in the compound heterozygous individual with an additional truncating variant were at the severe end of the spectrum in regard to motor milestones, speech delay, organic problems and pre- and postnatal growth of body and head, suggesting some genotype-phenotype correlation. Our study expands the phenotypic and molecular spectrum of EIF3F-related syndromic neurodevelopmental disorder.