Nevertheless, our findings overlap but are distinct from a previous study, which demonstrated that RLX could attenuate caspase-1 activity in an in vivo model of ischemia/reperfusion injury via an eNOS-dependent mechanism (Valle Raleigh et al., 2017), in which the direct involvement of the NLRP3 inflammasome was not provided (Valle Raleigh et al., 2017). This evidence concerns the gene NLRP3 and ischemia.