AKT1 and Miyoshi myopathy: As for the activation of the pro-survival pathways mediated by ERK1/2, AKT, and p38, Bor treatment was found to reduce the phospho-activation of ERK1 and/or ERK2 in all cell lines, had no significant effects on p38 phosphorylation levels, but increased the phosphorylation of AKT in the three human MM cell lines.