BTBD10 (BTB domain containing 10) is a nuclear protein that functions as a positive regulator of AKT signaling by inhibiting protein phosphatase 2A (PP2A)-mediated dephosphorylation of AKT, thereby maintaining AKT in its activated state 1. The protein contains a highly conserved BTB/POZ domain and is ubiquitously expressed with particularly high levels in brain, testis, and small intestine 2. BTBD10 promotes cell survival and proliferation through activation of the AKT/mTOR signaling pathway, as demonstrated by enhanced phosphorylation of both AKT and mTOR in pancreatic beta cells 3. The protein plays a critical role in motor neuron survival, as reduced BTBD10 expression leads to motor neuron death both in vitro and in vivo, and siRNA-mediated knockdown causes neuronal death in cultured motor neurons 1. Clinically, BTBD10 expression is significantly decreased in glioma tissues compared to normal brain tissue, with lower expression correlating with higher tumor grades 4. In sporadic amyotrophic lateral sclerosis (ALS), reduced BTBD10 expression in anterior horn cells is associated with Golgi apparatus fragmentation and phosphorylated TDP-43 inclusions, suggesting involvement in ALS pathogenesis 5. These findings establish BTBD10 as a crucial regulator of cell survival and proliferation with significant implications for neurological diseases and cancer.