BAX and osteogenesis imperfecta: The increase in the expression of pro-apoptotic proteins (Bax, CHOP and active caspase 3) in OI cells and their significant reduction or even normalization in the presence of RE, may unequivocally indicate that the accumulation of mutant type I collagen caused such stress and despite the activation of UPR (with the exception of OI II), the degradation processes mediated by autophagy and the proteasome were disturbed.