Taken together, these findings identify CEBPB and CEBPD, but not ATF5 itself, as direct targets of DN-ATF5 and indicate that the selective apoptotic activity of DN-ATF5 on glioma and other cancer cells is mediated by direct interference with CEBPB and CEBPD function and, as is likely, by indirect suppression of ATF5 activity by depriving it of its hetero-dimerization partners CEBPB and CEBPD. Here, CEBPD is linked to cancer.