Moreover, the evaluation of paired tumor and blood samples before and after the third SAHA dose prior to administration of other antineoplastic therapy revealed the increased acetylation of alpha tubulin and the K69 (lysine 69) residue of hsp90, induction of the stress protein hsp70, induction of p27 and p21 expression, and downregulation of cyclin-dependent kinase (CDK) 4, confirming the effects of SAHA reported in preclinical studies [179,180]. This evidence concerns the gene TUBA1B and neoplasm.