TGFB1 and neoplasm: Our efforts were directed to clarifying: (i) the molecular mechanism(s) for recognizing dysfunctional mitochondria by M/A and altering their redox state in glioblastoma cells and tissues, without significantly affecting the homeostasis of healthy cells and tissues; (ii) the role of two key proteins, tNOX and TGF-β1, for the induction of oxidative stress in the tumor, as well as for changing the redox state of healthy tissues and their vulnerability to oxidative damage.