Taken together, these results suggest that endothelial cell dysfunction and cell death can be initiated by deregulation of homologous recombination through decreased RAD51 and BRCA1 and a switch to non-homologous end-joining, an error-prone DNA repair mechanism, leading to accumulation of DNA errors, mutations, rearrangements, and even chromosomal translocations, as seen in endothelial cells from plexiform lesions isolated from pulmonary arterial hypertension patients13,14,66–68. This evidence concerns the gene RAD51 and pulmonary arterial hypertension.