The conversion of a bacterium from a non-pathogenic to a pathogenic existence is usually associated with the acquisition of virulence factors, the genes of which gain entry through bacteriophage infection, transposable elements or plasmid transfer. Pathogenesis research is mostly focused on how these factors enable the bacterium to infect the host or evade the repertoire of host defenses. Less effort is expended on understanding how the invading genes are affected by the complex regulatory circuits of the bacterium and how virulence is the result of converting these regulatory circuits to make them complicit with pathogenesis. An example of such a conversion is seen in Bacillus anthracis, and how acquired plasmid regulatory functions affect the activity of the regulatory processes of the bacterium, and vice versa, is now being revealed.