Xia et al. (2017) found that Drp1 and its Ser-616 phosphorylation were significantly increased in DCM patients and demonstrated that the use of LCZ696 against DOX-induced cardiac dysfunction is associated with alleviated Drp1-mediated mitochondrial dysfunction. Similar to our results, we focused on the anti-inflammatory effect of LCZ696. Our data indicated that LCZ696 prevented IκBα degradation, inhibited the nuclear translation of NF-κB and reduced the expression of inflammatory cytokines in vivo and in vitro. Here, NFKB1 is linked to familial dilated cardiomyopathy.