As noted before (Section 2.1.2), functional mitochondria stimulate NRF2 function by increasing mtROS [42]; (3) functional mitochondria assist MDR by providing sufficient ATP for ATP-dependent efflux pumps [98]; (4) in breast cancer cells, mitochondria increased doxorubicin resistance by inducing cell cycle arrest [99]; and, as alluded to above (Section 2.2.1), (5) mitochondria can help to create doxorubicin-resistance by mediating TME acidification [53]. This evidence concerns the gene NFE2L2 and breast carcinoma.