Since ErbB2 requires continuous association with HSP90 molecular chaperone for its stability and function as an oncogenic driver, the authors hypothesized that the HSP90/HSC70-interacting negative co-chaperone and E3 ubiquitin ligase CHIP/STUB1, whose expression is lost in most ErbB2-overexpressing breast cancers, provides one such mechanism. The gene discussed is ERBB2; the disease is breast cancer.