Extensive examinations indicated that, unlike the ameliorated AB-induced hypertrophic pathologies in the Sike-TG mice, the extent of cardiac hypertrophy and fibrosis in the Sike-M TG mice was similar to that in the NTG mice, as evidenced by the increased heart and cardiomyocyte sizes, aggravated cardiac dysfunction, exacerbated extent of fibrosis and elevated expression of fetal cardiac genes compared with the Sike-TG mice 8 weeks after AB surgery (Fig. 11e–j and Supplementary Fig. 7d,e). The gene discussed is SIKE1; the disease is cardiac hypertrophy.