They found that the increase in telomerase activity induced by IL-6 was demonstrated to occur through AKT-mediated phosphorylation of hTERT in MM cell lines, without any variation observed in the expression of hTERT at the mRNA or protein level (40), suggesting that the biological mechanism employed by MSCs to maintain their telomere length in an inflammatory cytokine-rich microenvironment, such as IL-6, may also be utilized (39). Here, AKT1 is linked to Miyoshi myopathy.