From functional analysis, we found that NAP1L2 exhibited higher expression in HG-stimulated CF, and knockdown of NAP1L2 ameliorated HG-induced proliferation, oxidative stress, inflammatory response and myofibroblast transformation of CF, indicating that NAP1L2 might be a stimulator for CF activation during the development of DCM. The gene discussed is NAP1L2; the disease is familial dilated cardiomyopathy.