Expression by these sensory neuron glial cells was notable because of the potential overlap of TEP-1 with CFH-1, previously identified on the surface of CEP neurons and phasmid sheath glia (Phsh) (14), and because a central element of the alternative complement pathway and AMD and EODM pathogenesis is thought to be a defect in CFH-mediated regulation of C3, a TEP-1-related thioester protein. This evidence concerns the gene TEP1 and age-related macular degeneration.