These HSPB1 mutants were chosen because they are located in the α-crystallin domain of HSPB1, previously identified as a ‘hot-spot’ in relation to small HSP (sHSP)-associated neuropathies,30 and reported to cause CMT.31 Although cells overexpressing WT HSPB1 were significantly resistant to ER stress, functional analysis revealed that all mutants failed to protect cells from TG-induced apoptosis (Figures 3b–d), exhibiting no difference in Annexin V staining (Figure 3b), Δψm (Figure 3c) or caspase-3 cleavage (Figure 3d) between TG-treated cells overexpressing HSPB1 mutants and EV controls. Here, CASP3 is linked to neuropathy.