During our investigations into the signalling pathways responsible for SIKE-regulated pathological cardiac hypertrophy, we demonstrated that the activation of AKT signalling was dramatically suppressed by SIKE upon hypertrophic stress, and the necessity of AKT signalling for the functional role of SIKE in cardiac remodelling was evidenced by the ability of artificial overexpression of Akt to reverse the beneficial effect of Sike on cardiomyocyte enlargement. The gene discussed is SIKE1; the disease is cardiac hypertrophy.