Because our compounds can prevent intracellular replication of C. trachomatis when present throughout infection, and EB formation is a late event that occurs once RBs have ceased to replicate, we were not surprised to see that c1e–c5e and c1v–c5v abrogated EB formation by CTL2-GFP in HeLa cells (Fig 5B and S7A Data). The gene discussed is SLC44A2; the disease is infection.