In the FD sham and FD/LCS mice compared with the control counterparts, activation of lungs’ mTORC1 signaling cascade was evident with up-regulation of the upstream mediator, phosphorylated Akt (p-Akt), which activates phosphorylation of mTORC1 (mechanistic target of rapamycin) kinase and its downstream effector, the ribosomal p70-S6 kinase (pS6k), to stimulate ribosomal activity for protein biosynthesis and the signaling target of hypoxia-inducing factor (HIF-1α) [38]. Here, HIF1A is linked to Fabry disease.