Considering that Bok, the third effector protein of the family, low expressed in MM [94], and the results derived from dual-gene suppression of Bax and Bak, we conclude that the main cytotoxic mechanism triggered by alisertib at high doses and by barasertib is the mitochondrial apoptotic pathway, while alisertib at low doses activates an alternative Bax/Bak-independent cell death mechanism, in contrast with other reports on colorectal cancer [93] and Burkitt lymphoma [95]. This evidence concerns the gene BOK and Miyoshi myopathy.