ERBB2/HER2 is one of the most sensitive client proteins of HSP90 [6,7], and 17-AAG has been shown to cause depletion of ERBB2/HER2 leading to significant growth inhibition in ERBB2/HER2 overexpressing breast cancer cells and tumour xenografts [8], and more importantly to cause regression in trastuzumab-refractory ERBB2/HER2 positive breast cancer patients [1-3]. Here, ERBB2 is linked to neoplasm.