In this context, Zhao et al. demonstrated in a CCM mouse model that CD73(5’-NUCLEOTIDASE, ECTO-5’-NUCLEOTIDASE)-mediated hydrolysis of extracellular ATP to adenosine plays a pivotal role in suppressing excessive inflammation and reducing myocardial apoptosis, thereby highlighting the therapeutic potential of CD73(5’-NUCLEOTIDASE, ECTO-5’-NUCLEOTIDASE) in modulating inflammation-associated cardiac injury [66]. This evidence concerns the gene NT5E and cerebral cavernous malformation.