AKT1 and Miyoshi myopathy: As shown in Fig. 5a-b, phosphorylation of both p70S6K (a substrate of the mTORC1 complex) and AKT-ser473 (a substrate of the mTORC2 complex) was increased in HMGB1-knockdown MM cells compared to control cells, suggesting that both pathways were activated after HMGB1 knockdown.