This unexpected scenario would imply that GSK-3, at basal conditions (to a lesser extent) and in the presence of BZ (to a larger extent), might positively regulate the PI3K/AKT pathway, which in turn is a negative regulator of GSK-3 - as also suggested by the significant amount of GSK-3 (especially GSK-3β) Ser-phosphorylation found in MM cells (Fig. 1A and 6D). The gene discussed is AKT1; the disease is Miyoshi myopathy.