Compared with the alleviated phenotypes in the pressure overload-induced USP38cko, TBK1 overexpression in the heart reduced the protective effect of USP38cko in AB-induced cardiac remodeling, along with increased HW, HW/BW, HW/TL and LW/BW ratio (Figure 9D), exaggerated cardiac dysfunction (Figure 9E), larger myocyte cross-sectional area (Figure 9F), aggravated myocardial fibrosis (Figure 9G), and increased TBK1/Akt signaling protein levels (Figure 9H). Here, AKT1 is linked to Myocardial fibrosis.