HDAC6 and esophageal squamous cell carcinoma: In one hand, HDAC6 could deacetylate HSP90 and thus stabilized many oncogenic proteins, inhibition of HDAC6 strengthens the binding of HSP90 to 17‐AAG; on the other hand, HDAC6 itself is a client protein of HSP90 and its activity is upregulated by EGFR, another client protein of HSP90.22, 23, 24 We found that co‐administration of Tubastatin A and PU‐H71 greatly suppressed both proliferation and migration in ESCC cells examed.