Abnormalities in ASM bioactivity result in disturbed sphingomyelin degradation and ceramide generation, leading to extreme accumulation of sphingomyelin but deficient ceramide production.1, 13 Aberrant ASM-dominated sphingomyelin-ceramide signaling is associated with numbers of human nervous disorders including Alzheimer disease, Parkinson disease, schizophrenia,and depression.13 In particular, ASM deficiency contributes to lipid storage disorders, i.e., Niemann–Pick disease.11, 14. The gene discussed is SMPD1; the disease is Parkinson disease.