C-Jun-N-terminal-kinases (JNKs), members of the mitogen-activated-protein-kinase family, are significantly linked with neurological and neurodegenerative pathologies and cancer progression. However, JNKs serve key roles under physiological conditions, particularly within the central-nervous-system (CNS), where they are critical in governing neural proliferation and differentiation during both embryogenesis and adult stages. These processes control the development of CNS, avoiding neurodevelopment disorders. JNK are key to maintain the proper activity of neural-stem-cells (NSC) and neural-progenitors (NPC) that exist in adults, which keep the convenient brain plasticity and homeostasis. This review underscores how the interaction of JNK with upstream and downstream molecules acts as a regulatory mechanism to manage the self-renewal capacity and differentiation of NSC/NPC during CNS development and in adult neurogenic niches. Evidence suggests that JNK is reliant on non-canonical Wnt components, Fbw7-ubiquitin-ligase, and WDR62-scaffold-protein, regulating substrates such as transcription factors and cytoskeletal proteins. Therefore, understanding which pathways and molecules interact with JNK will bring knowledge on how JNK activation orchestrates neuronal processes that occur in CNS development and brain disorders. © 2024 The AuthorsInstituto Tecnológico y de Estudios Superiores de Occidente, Universidad Jesuita de Guadalajara; Generalitat de Catalunya, (2021 SGR 00288); Generalitat de Catalunya; Institute of Neurosciences UB, (UB-LE-9035, CEX2021-001159-M, UB-LE-9115); Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, CIBERNED, (CB06/05/2004); Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, CIBERNED; Ministerio de Ciencia, Innovación y Universidades, MCIU, (PID2021-123462OB-I00); Ministerio de Ciencia, Innovación y Universidades, MCIU