Under pressure overload, VCP expression was decreased in the hearts of WT mice and the inhibitory binding of VCP with AKT at T308 was removed, which allows AKT to become phosphorylated by PI3K/PDK1 on threonine 308, then subsequently activating mTORC1 signaling and inducing cardiac hypertrophy. The gene discussed is PDK1; the disease is cardiac hypertrophy.