One study performed in RAW264.7 cells at a high multiplicity of infection (MOI) concluded that infection blocked IFNγ-mediated STAT1 phosphorylation, likely via upregulation of suppressor of cytokine signaling-1 (SOCS1) [39], while another study implicated partial STAT1 dephosphorylation in the nuclei of infected human fibroblasts [40]. This evidence concerns the gene STAT1 and infection.