Through molecular analysis, the researchers also identified the specific signaling pathway regulated by MOTS-c, demonstrating for the first time "that MOTS-c modulates the CK2-PTEN-AKT-FOXO1 pathway to inhibit myostatin expression and muscle wasting," and suggesting that the exercise mimetic effect of MOTS-c may be derived from its previously unknown role as a myostatin inhibitor, according to the paper.