We have previously shown the nuclear DDR and the CDSP pathways are activated in the mouse models of dilated cardiomyopathy (DCM) caused by deficiency of the nuclear envelope proteins, including LMNA and TMEM43, or the cardiac-myocyte restricted expression of the mutant LMNAD300N protein, the latter is known to cause non-syndromic cardiac progeria in humans[11–14]. Here, SLC22A5 is linked to dilated cardiomyopathy.