When these findings are considered together with prior reports that (i) fragmented Golgi exhibit accelerated anterograde trafficking (1), (ii) GRASP phosphorylation or depletion increases Golgi anterograde trafficking (7, 107), (iii) MVBs receive anterograde traffic from the TGN (45), and (iv) A. phagocytophilum not only lives in a pathogen-modified MVB but also parasitizes TGN-derived vesicles that are delivered into the ApV lumen (25, 44), the essentiality of C1P to the bacterium’s infection cycle becomes clear. The gene discussed is TAMALIN; the disease is infection.