A previous study found that STAT5A recruits HDAC1 and activates the transcription of inhibitor of differentiation-1 (ID-1) via deacetylating transcription factor CEBPB in murine pro-B cells.66 Consistently, we found that STAT5A recruits HDAC1 and HDAC2 in NPC-derived cells. This evidence concerns the gene STAT5A and nasopharyngeal carcinoma.