Forkhead box protein P2 (FOXP2) is a well-studied gene known to play an 
essential role in normal speech development. Deletions in the gene have been 
shown to result in developmental speech disorders and regulatory disruption of 
downstream gene targets associated with common forms of language impairments. 
Despite similarities in motor planning and execution between speech development 
and oral feeding competence, there have been no reports to date linking 
deletions within the FOXP2 gene to oral feeding impairments in the newborn. The 
patient was a nondysmorphic, appropriately and symmetrically grown male infant 
born at 35-wk gestational age. He had a prolonged neonatal intensive care unit 
stay because of persistent oral feeding incoordination requiring gastrostomy 
tube placement. Cardiac and neurological imagings were within normal limits. A 
microarray analysis found an ∼9-kb loss within chromosome band 7q3.1 that 
contains exon 2 of FOXP2, demonstrating a single copy of this region instead of 
the normal two copies per diploid gene. This case study expands our current 
understanding of the role FOXP2 exerts on motor planning and coordination 
necessary for both oral feeding success and speech-language development. This 
case report has important consequences for future diagnosis and treatment for 
infants with FOXP2 deletions, mutations, and varying levels of gene expression.