In contrast, in CKD patients, reduced IGF-1 levels further impaired the PI3K/Akt/mTOR pathway-mediated protein synthesis and enhanced the PI3K/Akt/FOXO pathway, concomitant with the activation of the ubiquitin-proteasome system, which targets the degradation of muscle fibrous proteins (63–65). This evidence concerns the gene IGF1 and chronic kidney disease.