Likewise, hearts lacking ADAR1 showed severe myocyte disarray that is accompanied with a significant increase of interstitial fibrosis (Figures 1G,J), revealing intricate features of clinical heart failure including potent re-activation of stress-induced genes such as Acta1, Nppb, Myh7, and Nppa in the tamoxifen-treated αMHC-MCM-ADAR1F/F mice (Figure 1K). The gene discussed is ACTA1; the disease is heart failure.