AKT1 and Miyoshi myopathy: Therefore, the increase in RUNX2 expression in MM cells could be sustained, also, by other pathways (not only those related to the Wnt/β-catenin axis [61]), such as the PI3K/AKT cascade [60,62] or soluble factors and adhesion molecules involved in MM–MSC cross-talk, as reported in [15,63].