Considering our previous data showing activation of the nuclear component of the DDR pathway, namely the H2AFX/ATM/TP53 pathway in humans with primary DCM, we speculate that activation of CGAS is likely due to increased DSBs in the genomic DNA and the release of genomic DNA into the cytosol[11–13]. The gene discussed is ATM; the disease is familial dilated cardiomyopathy.