Moreover, cardiac-specific deletion of LKB1, a master serine/threonine kinase to phosphorylate and activate AMPK [65], leads to cardiac hypertrophy and dysfunction in mice, accompanied by reduced AMPK phosphorylation and increased phosphorylation of p70S6 kinase, which can regulate global protein synthesis [49, 66]. The gene discussed is PRKAA2; the disease is cardiac hypertrophy.