ERBB2 and breast carcinoma: These findings imply that loss of CHIP, which is seen in a majority of EbB2-overexpressing breast cancers [35], accentuates ErbB2-driven oncogenesis in part by ensuring that HSP90 remains associated with ErbB2 and allows this complex to exit the ER/Golgi for transport to the cell surface where it functions to promote oncogenesis.