Cancer and neurodegeneration include a group of diseases that are mechanistically distinct but may share common therapeutic targets. Both cancer and neurodegeneration may propagate by contiguity, leading to disease spread from one body part to another. Autophagy is a common quality control mechanism shared by mitotic and post-mitotic cells and it can be exploited to accelerate clearance of unwanted oncogenes and reduce accumulation of toxic proteins in cancer and neurodegeneration, respectively. Tyrosine kinase inhibition is a therapeutically relevant strategy that can induce autophagy, leading to normal cell survival in certain type of cells. This perspective provides insights into how tyrosine kinase inhibition can be clinically used to arrest mitotic cell division and tumor growth, while promoting survival of post-mitotic neurons. As modulators of myeloid cells, TKIs may also positively regulate neuronal death and produce neuro-restorative effects, independent of brain concentration, via production of necessary growth factors and proliferation of myeloid-derived glial cells. Autophagictoxic protein clearance and production of growth factors may restore fluctuations of neurotransmitters, leading to alterations of motor and cognitive functions. Tyrosine kinase inhibition provides a double-edge sword via manipulation of autophagy to inhibit cell division and tumor growth in cancer on one hand, and promote toxic protein degradation and neuronal survival in neurodegeneration on the other hand.