Further studies in mice with cardiomyocyte-specific deletion of the GR revealed aberrant regulation of a large cohort of genes associated with cardiovascular disease as well as unique disease genes associated with inflammatory processes, and demonstrated that a deficiency in cardiomyocyte glucocorticoid signaling leads to spontaneous cardiac hypertrophy, heart failure, and death, indicating an obligate role for the GR in maintaining normal cardiovascular function [49]. Here, NR3C1 is linked to cardiac hypertrophy.