TUDCA mediates mitochondria-cell cycle retrograde signals to regulate NSC fate. The NSC modulatory properties of TUDCA result from inhibition of differentiation-induced mitochondrial apoptotic events by the bile acid, and from subsequent decrease in ROS and ATP mitochondrial levels. This, in turn, contributes for the enhancement of both NSC proliferation and neuronal rather than astroglial conversion of differentiating NSCs. Importantly, TUDCA-mediated effects in increasing NSC pool and lineage determination occur in a mitochondrial redox state- and ATP-dependent manner. Interactions that were described, suggested or shown indirectly are depicted.