Garcia-Garcia et al. (2009) were able to connect the activity of the human HDAC1 with the infection process of Anaplasma phagocytophilum in THP-1 cells (granulocyte model). Hereafter, the infection process led to an increased activation of HDAC1 leading to a reduced histone H3 acetylation and to the silencing of host defense genes. In accordance, the inhibition of HDAC1 by siRNA led to a significant drop of the bacterial load. This shows that the epigenetic control of the host cell by the bacterium promotes the disease by increased survival of the pathogen (Garcia-Garcia et al., 2009). The gene discussed is HDAC1; the disease is infection.