TAFA2 is a neurotrophic factor essential for neuronal survival and cognitive function. Primarily expressed in the central nervous system, TAFA2 functions as a secreted signaling molecule that prevents neuronal apoptosis through multiple mechanisms 1. The protein directly binds to ADGRL1 (adhesion G protein-coupled receptor L1) via its lectin-like domain, activating the cAMP/PKA/CREB/BCL2 anti-apoptotic pathway 1. TAFA2 also promotes neuronal survival through PI3K/Akt and MAPK/Erk signaling, with downstream effects on CREB target genes including BDNF 2. Beyond neuronal cells, TAFA2 regulates mesenchymal stem cell migration via Rac1-p38 pathway activation, supporting tissue repair processes 3. In disease contexts, TAFA2 deficiency impairs spatial learning, memory, and emotional regulation 2, while dysregulation associates with asthma exacerbation susceptibility 4 and epilepsy pathogenesis 5. Additionally, neuron-derived TAFA2 plays a dual role in liver inflammation by recruiting CCR2+ macrophages during ischemia-reperfusion injury, a mechanism suppressible by sour taste signaling 6. These findings identify TAFA2 as a critical neuroimmune mediator relevant to neurological and inflammatory disorders.