Grounded on our previous studies showing that EV-Cx43 facilitates the communication with acceptor cells and because post-infarction circulating EVs exacerbate inflammatory responses, contributing to impaired heart function, we can speculate that reduced Cx43 levels prevent the spreading of certain metabolites or signaling molecules, constituting a cardioprotective mechanism (Soares et al, 2015; Biemmi et al, 2020). Here, GJA1 is linked to infarction.