Altogether, these data demonstrate that the infection cycles of C. trachomatis and C. pneumoniae are less susceptible to pharmacologic inhibition of ASM than A. phagocytophilum or C. burnetii, which is due, at least in part, to the abilities of these bacteria to hijack cholesterol from the Golgi and MVBs and to parasitize other lipids such as sphingomyelin. The gene discussed is SMPD1; the disease is infection.