From a pathophysiological perspective an interesting role of SPPL3 was recently reported at the tumour-CD8+ T cell interface, since experimental loss of SPPL3 in tumour cells leads to diminished CD8+ T cell activation through a glycosphingolipid-dependent mechanism [24] and sub-clonal loss of SPPL3 in a variety of cancers appears to be associated with a less pronounced T cell response [26]. The gene discussed is SPPL3; the disease is neoplasm.