It is also possible that S6K1 disruption is inducing changes in the signaling network through its regulation of the insulin/IGF-1 signaling network (Johnson et al., 2013a) or additional targets, or that S6K1 disruption is alleviating mitochondrial disease in these animals by a mechanism distinct from rapamycin. Here, RPS6KB1 is linked to inborn mitochondrial metabolism disorder.