MBLAC1 (metallo-beta-lactamase domain containing 1) is an endoribonuclease that catalyzes 3' end processing of histone pre-mRNA during S-phase of the cell cycle 1. The enzyme cleaves histone pre-mRNA at specific sites downstream of stem-loop structures, recognizing sequences including 5'-ACCCA-3' and 5'-ACCCACA-3', with the HDE element preventing non-specific cleavage 1. This histone mRNA processing function is essential for cell cycle progression, particularly S-phase entry and progression 1. MBLAC1 depletion significantly impairs cell cycle progression, identifying it as a potential S-phase-specific cancer target 1. Beyond cell cycle regulation, MBLAC1 has emerged as a neurodegenerative disease risk factor, with mutations in its C. elegans ortholog swip-10 causing dopamine-dependent motor dysfunction and neuronal degeneration 2. In humans, MBLAC1 variants jointly associate with Alzheimer's disease and cardiovascular risk factors, particularly lipid abnormalities 3. MBLAC1 loss results in tissue-specific metabolic perturbations including reduced hepatic NADH levels, increased redox oxidation, and elevated serum glucose, suggesting mitochondrial dysfunction 45. These metabolic changes may link peripheral comorbidities to neurodegeneration in MBLAC1-associated disease.