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It involves anatomical abnormalities that change the normal flow of blood through the heart resulting in low oxygenation. Although not all of the underlying causes of TOF are completely understood, the disease has been associated with varying genetic etiologies including chromosomal abnormalities and Mendelian disorders, but can also occur as an isolated defect. In this report, we describe a familial case of TOF associated with a 1.8\u2009Mb deletion of chromosome 10p11. Among the three genes in the region one is <jats:italic>Neuropilin1 (NRP1)<\/jats:italic>, a membrane co\u2010receptor of <jats:italic>VEGF<\/jats:italic> that modulates vasculogenesis. Hemizygous levels of <jats:italic>NRP1<\/jats:italic> resulted in a reduced expression at the transcriptional and protein levels in patient\u2010derived cells. Reduction of NRP1 also lead to decreased function of its activity as a co\u2010receptor in intermolecular VEGF signaling. 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