Similarly, for chronic CLL cells with apoptosis resistance caused by impaired Bax/Bak protein activation, DT-061 treatment triggers apoptosis via the induction of permeability transition pores in the mitochondria (mPTPs), which increases the expression of cleaved caspase-9 and cleaved PARP, independent of the Bax/Bak pathway 173. Here, BAK1 is linked to B-cell chronic lymphocytic leukemia.