In this context, the C-terminal HSP90 inhibitor NCT-547 (Table 1) was found to: (1) induce apoptosis and target HER2 signaling; (2) promote the degradation of FL-HER2 and truncated p95HER2 in cells properly engineered to ectopically express both molecules; (3) inhibit tumor growth in trastuzumab-resistant JIMT-1 xenografts; and (4) reduce ALDH1 activity, the CD44high/CD24low subset and MFE, both in vitro and in vivo [50]. Here, ALDH1A1 is linked to neoplasm.