Interestingly, a study carried out on immortalized and undifferentiated myoblast cells from DMD patients, harboring mutations leading to prematurely truncated dystrophin, showed an accumulation of ubiquitinated protein aggregates containing HpsB5, a chaperone, which is known to protect key elements for muscle contractile function [56,57]. The gene discussed is DMD; the disease is Duchenne muscular dystrophy.