ERBB2, present at low levels in normal cells, is overexpressed in cancer cells with ERBB2 gene amplification, leading to growth factor-independent activation of ERBB2 signaling through formation of ERBB2 homodimers (Pickl and Ries 2009, Maadi et al. 2018). It is assumed that during homodimerization, similar to normal heterodimerization with ligand-activated ERBB family members, chaperone proteins HSP90 and CDC37, as well as ERBB2IP, dissociate from ERBB2 (Borg et al. 2000, Xu et al. 2001, Citri et al. 2004).