Our functional data are consistent with this hypothesis: in hematologic tumor models, silencing UNC13B reduced proliferation and enhanced apoptosis, accompanied by the downregulation of mitochondrial quality control (e.g., PINK1) and cell cycle factors (e.g., CDK2), suggesting that UNC13B supports tumor cell survival through a “secretion/exocytosis–mitochondrial stress–cell cycle” axis. Here, UNC13B is linked to neoplasm.