We and others demonstrated that proteasomal dysfunction induced by knockout of the immunoproteasome subunits β1i, β2i, or β5i in mice attenuated PTEN degradation, leading to the downregulation of AKT-associated signaling pathways in ischemic hearts and AF (Cai et al., 2008; Li et al., 2018, 2019). The gene discussed is AKT1; the disease is atrial fibrillation.