ASAH2B encodes N-acylsphingosine amidohydrolase 2B, a key enzyme in ceramide metabolism 1. As a neutral ceramidase, ASAH2B processes N-acylsphingosine lipids, playing a central role in sphingolipid homeostasis 1. The enzyme is highly expressed in visceral organs including heart, liver, kidneys, lungs, and stomach, but shows minimal brain expression in normal conditions 1. ASAH2B has emerging disease relevance across multiple conditions. In Alzheimer's disease, serum ASAH2B/ASAH2 levels are significantly elevated in pre-symptomatic individuals and those with mild cognitive impairment, preceding clinical dementia onset 1. ASAH2B expression increases early in AD mouse models at three months before declining at 14 months, suggesting involvement in disease pathogenesis 1. Dysregulation of lipid trafficking and inflammatory pathways associated with altered ASAH2B indicates contributions to neurodegeneration mechanisms 1. In cancer, long noncoding RNA ASAH2B-2 is upregulated by the mTOR inhibitor everolimus in breast cancer cells, promoting cell proliferation and reducing therapeutic efficacy 2. Additionally, ASAH2B shows genetic association with gout susceptibility through genome-wide studies, implicating metabolic and immune pathways in hyperuricemia-related inflammation 3. These findings suggest ASAH2B as both a potential biomarker and therapeutic target across metabolic, neurodegenerative, and malignant diseases.