One possibility is that the activation of flhDC transcription from P5flhDC might represent a mechanism of protein amplification by a surge of transcription, when it is necessary to turn on the Spi1 regulatory network, even under conditions where flagella synthesis is inhibited at the level of fliA and fliC. This scenario can be very useful after infection when the bacteria requires expression of virulence factors to survive the physical and immune clearance of the eukaryotic host. The gene discussed is SPI1; the disease is infection.