We further validated this experimentally in a doxorubicin-induced murine DCM model, demonstrating significant increases in the DNA double-strand break marker γ-H2AX, checkpoint kinase Chk2, multiple DNA repair pathway components (Ogg1, Xpc, Brca1, Ku70), and downstream effectors like p21 and Bax 78-81. The gene discussed is BAX; the disease is familial dilated cardiomyopathy.