The TDRD3–USP9X interaction is not only important for preventing TDRD3 ubiquitination and degradation, but is also essential for stress-induced localization of USP9X to SGs and USP9X DUB activity towards the anti-apoptotic protein MCL-1, both of which could be the molecular mechanisms that explain the observation that TDRD3 knockdown sensitizes cancer cells to apoptosis (Figure 7f). The gene discussed is MCL1; the disease is cancer.