Loss of normal PLZF function in myeloid cells bearing the t(11; 17) is part of the oncogenic mechanism in acute promyelocytic leukemia development [13–15] while loss of expression of PLZF in melanoma [16], and a wide variety of solid tumors, including breast, prostate and glioblastoma (http://www.oncomine.org), suggest that PLZF may be a bona fide tumor suppressor. Here, ZBTB16 is linked to acute promyelocytic leukemia.