PRKDC and familial dilated cardiomyopathy: DDR, traditionally regarded as a protective mechanism for maintaining genomic stability,[8] can paradoxically lead to cell death under conditions of sustained or excessive DNA damage.[9] In metabolic diseases like diabetes, chronic DDR activation may promote cellular senescence and cardiomyocyte dysfunction, implicating DDR as a key driver of DCM.[10] Our previous studies have demonstrated that DNA‐PKcs contributes to cellular apoptosis in septic cardiomyopathy[11] and ischemia‐reperfusion injury,[12] suggesting a similar role in DCM.