Previously, we have shown that this requirement is lost in PAX3-FKHR, the product of a t(2;13) chromosomal translocation associated with alveolar rhabdomyosarcoma.     ///    "Furthermore, we could abolish the homeodomain-dependent transcription and transforming activities of PAX3-FKHR by replacing its FKHR transactivation domain with Pax3 transactivation domain. "    ///    "In contrast to Pax3, the chimeric PAX3-FKHR, which acts as an oncogene, can efficiently activate a DNA sequence element containing only a homeodomain binding site (TAATAN(2-3)ATTA), despite the presence of an intact Pax3 paired domain. "