However, in the muscle of Dox-treated Tg(HQK) mice, only a marginal increase in BAX expression was observed whereas significant over-expression of other p53 regulated pro-apoptotic proteins, including BAK1, BBC3 and PMAIP1, and MCL1, were detected, suggesting that PrPC-mediated myopathy observed in this model may depend on Bax-independent pathways that involve BAK1, BBC3, PMAIP1, and MCL1. Here, BAX is linked to myopathy.