In contrast to the role of GSK3β in Abeta and hyperphosphorylated TAU-mediated toxicity, where the activation of GSK3 is pathological, Nicot et al. demonstrated that the lack of GSK3 catalytic activity directed toward T586 of the neighbor of BRCA1 (NBR1) caused the increased protein aggregation and stabilization of ubiquitinated proteins, and found that NBR1 phosphorylation on T586 is reduced in IBM [101]. Here, GSK3B is linked to inclusion body myositis.