New evidence indicates that cardiomyocytes from both patient cardiac samples and rodent heart disease models exhibit elevated expression of cGAS-STING pathway components [9, 22]; that cardiomyocyte-specific activation of STING led to the development of cardiac hypertrophy and failure in mice [22]; and that depleting or pharmacologically inhibiting cGAS-STING pathway players alleviates cardiac dysfunction and hypertrophy [9,22]. This evidence concerns the gene CGAS and heart disorder.