It was characterized to bind host DNA and nuclear proteins in 2004 (Park et al., 2004), and in 2009 it was shown to be the factor responsible for silencing granulocyte respiratory burst (Garcia-Garcia et al., 2009b) by recruiting histone deacetylase 1 (HDAC1) to alter granulocyte function with infection (Garcia-Garcia et al., 2009a; Rennoll-Bankert et al., 2015). The gene discussed is HDAC1; the disease is infection.