Furthermore, a genome-wide analysis of the PML-RARa/RXR binding site using Chip-seq in an APL cell line (NB4) and primary APL cells revealed that the PML-RARa /RXR dimer interacts with and represses a broader range of promoter regions than its RARa /RXR counterpart [57], likely contributing to the oncogenic action of the fusion protein [55]. The gene discussed is RARA; the disease is acute promyelocytic leukemia.