ASAH1 (N-acylsphingosine amidohydrolase 1) encodes acid ceramidase, a lysosomal enzyme that catalyzes the breakdown of ceramide to sphingosine in sphingolipid metabolism 1. This enzymatic function is critical for maintaining hepatic lipid homeostasis; hepatocyte-specific ASAH1 deletion exacerbates high-fat diet-induced steatosis, hepatitis, and fibrosis through accumulation of ceramide and cholesterol, impaired autophagy, and endoplasmic reticulum stress 2. ASAH1 also regulates immune responses; its inhibition in colorectal cancer induces immunological cell death and enhances anti-tumor immunity through type I/II interferon activation and cytotoxic T cell infiltration, making it a therapeutic target when combined with checkpoint inhibitors 1. In asthma, reduced ASAH1 expression correlates with enhanced CD8+ T cell and NK cell infiltration 3. Pathologically, ASAH1 mutations cause Farber lipogranulomatosis and related sphingolipidoses, while variants contribute to Parkinson's disease susceptibility through impaired lysosomal function 4. Podocyte-specific ASAH1 deletion disrupts TRPML1-mediated lysosomal calcium signaling, increasing exosome release and inducing nephrotic syndrome 5. ASAH1 genetic variants also interact with neurotrophin signaling in schizophrenia pathogenesis 6.