Acute promyelocytic leukemia (APL) is characterized by the translocation of the retinoic acid receptor (RAR) gene on chromosome 17q21 with the promyelocytic leukemia (PML) gene on chromosome 15q22, resulting in t(15;17). The chimeric PML-RARα receptor protein retains essential functional domains encoded by the two genes. PML-RARα blocks cellular differentiation, thereby inducing leukemogenesis. All-trans-retinoic acid (ATRA) induces differentiation of APL cells. It is thought that ATRA promotes PML-RARα degredation which allows differentiation to progress. ATRA-induced differentiation of APL cells involves the coordinated regulation of many genes. NB4, a cell line derived from an APL patient, expresses RIG-G (Retinoic acid Induced Gene G) protein following treatment with ATRA or IFN-α. RIG-G displays strong homology to the protein products of the IFN-stimulated gene (ISG) family and contains multiple sites for post-translational modification. However, these sites remain to be fully characterized. Thus, RIG-G may be a component of ATRA and IFN signaling pathways that mediate cellular differentiation and the avoidance of leukemogenesis.