For example, in Ang II-induced cardiac hypertrophy, activation of immunoproteasomes was found to promote degradation of MKP-1 and IκBα and subsequent activation of STAT1 and NF-κB, thereby leading to Th1 cell differentiation and cardiac remodeling (Qin et al., 2018); while in DOCA/salt-induced cardiac hypertrophy, the immunoproteasome LMP10 subunit was shown to activate IκBα/ NF-κB and TGF-β1/Smad2/3 signaling to facilitate cardiac fibrosis and inflammation (Yan et al., 2017). The gene discussed is SMAD2; the disease is fibrosis.