In contrast with the ameliorated phenotypes in the Sike-TG4 mice compared with the NTG mice, individual Tbk1 or double Sike and Tbk1 overexpression in the heart promoted AB-induced cardiac hypertrophy and fibrosis, along with increased HW/BW, LW/BW and HW/TL ratios (Fig. 9g–i), worsened cardiac function (Supplementary Fig. 6g), larger heart and cardiomyocyte sizes (Fig. 9j,k), aggravated fibrosis (Fig. 9j,l) and increased transcript levels of fetal cardiac genes (Supplementary Fig. 6h). The gene discussed is SIKE1; the disease is cardiac hypertrophy.