RPTOR and Cachexia: The increase in autophagic flux in Raptor ko mice during cachexia can be interpreted in two ways: (i) the induction of autophagy during cachexia is independent of mTORC1, and (ii) the reduction in mTORC1 is responsible for the induction of autophagy during cachexia, but the more pronounced reduction in mTORC1 signalling after genetic loss of function leads to an even further increase in autophagic flux through the same signalling pathway.