We aim to understand the underlying factors that contribute to the increased incidence of Congenital Heart Defects (CHDs) in individuals with Down Syndrome. We are trying to determine if the altered adhesiveness of cells with T21 results in hyperactivated mechanosensitive pathways, increased cellular contractility, altered morphogenesis and increased force transmitted to the nucleus, which all have the potential to influence gene expression and may help elucidate underlying factors that contribute to CHD.