This may be explained by feedback effects of mTORC1 inhibition on the PI3K/Akt pathway and mTORC2, or effects on autophagy, which is also modulated by VCP.27, 42, 55, 64 The findings may be clinically relevant, as some approaches to improve cancer therapy aim to reduce the activity of pathways that promote protein synthesis, such as mTORC1.68 Our results suggest that such a strategy may not be beneficial when combined with proteotoxic treatment approaches such as VCP inhibition. The gene discussed is VCP; the disease is cancer.