As an example, patients with Niemann–Pick disease, who have mutations in the ASM gene, exhibit neurological symptoms at early age, and develop visceral organ abnormalities in later life.4 Patients with Niemann–Pick disease are at risk of infections,5 as can be modeled in ASM-deficient mice.6, 7 This phenotype has been attributed to phagocyte dysfunction.8 Recently, however, ASM function has also been described and noted in various other non-phagocytic immune cells, for example, regulating cytotoxic granule secretion by CD8+ T cells.9 This evidence concerns the gene SMPD1 and Niemann-Pick disease.