Consistent with the in vitro characterization shown earlier, both types of tumor expressed BAK (Figure 5C) and demonstrated comparable depletion of the HSP90 client protein ERBB2 and induction of HSP72 in response to 17-AAG treatment in vivo (Figure 5D) indicating comparable HSP90 target engagement in each member of the isogenic pair. The gene discussed is BAK1; the disease is neoplasm.