These alterations could be prevented with adenosine deaminase therapy or by genetic deletion of the A2BAR, indicating that (a) the elevated placental adenosine could be attributed to its impaired elimination, (b) the effects of adenosine were mediated by A2BAR, and (c) adenosine deaminase was the key enzyme responsible for initiating the underlying biochemical changes of clinical preeclampsia and fetal programming [146]. Here, ADA is linked to preeclampsia.