With the lack of Klf14-mediated apoA-I promoter activation, hepatic-specific Klf14 deletions in Apoe−/− mice cause marked acceleration of atherosclerotic lesion development in combination with decreased high-density lipoprotein (HDL) cholesterol levels, and cholesterol efflux, whereas Klf14 activation reduces atherosclerosis [11]. The gene discussed is KLF14; the disease is atherosclerosis.