The mouse model of cardiac hypertrophy demonstrated reduced cardiac cross-sectional area and inflammatory response due to STING deletion, which also inhibited phosphorylation of ER stress markers, including protein kinase RNA (PKR)-like ER kinase (PERK), inositol-requiring enzyme 1α (IRE-1α), and eukaryotic translation initiation factor 2α (eIF2α). Here, STING1 is linked to cardiac hypertrophy.