A hypothetical mechanism by which condition-specific or non-specific transcriptional responses to IFN-γ may be achieved. (A – D) Condition-specific responsiveness to IFN-γ of a gene, "gene 1". Condition A: STAT1 ("S") and transcription factor-X ("X") are inactive, and hence the binding sites for STAT1 (blue DNA) and X (yellow DNA) are unoccupied. In this state, chromatin-modifying proteins render regions near the binding sites for STAT1 and X (red DNA) inaccessible to RNApolII. Condition B: In this condition, STAT1 is activated by IFN-γ, and associates with its binding site upstream of gene 1. STAT1 recruits chromatin-modifying proteins ("?") to make the region accessible to RNApolII; STAT1 then recruits RNApolII to DNA near the STAT1 binding site. RNApolII is unable to transcribe gene 1, however, because the chromatin configuration near the binding site for X inhibits its progression. Condition C: In this condition, X is active, and associates with its binding site upstream of gene1 to recruit chromatin-modifying proteins, which make the region accessible to RNApolII. However, RNApolII is not actively recruited to the gene 1 promoter, so gene 1 is not transcribed. Condition D: In this condition, both STAT1 and X associate with their binding sites, and recruit chromatin-modifying proteins to make the promoter accessible to RNApolII. STAT1 then recruits RNApolII, and RNApolII is able to progress along the promoter to transcribe gene 1. (E) Non-specific transcriptional responsiveness to IFN-γ of a gene, "gene 2". Gene 2 is regulated by transcription factors that associate with binding sites (blue, yellow and purple DNA) within its promoter. Gene 2 has a key role in regulating the response to IFN-γ, so it is important that it is induced by IFN-γ in all tissues, under all conditions. The STAT1 binding site is therefore located close to the start of gene 2, where other regulatory elements within the promoter will not affect the ability of STAT1 to induce transcription of gene 2.