Transcriptional inactivation of one copy of the X chromosome in female cells equalizes expression of X-linked genes between males and females. This "dosage compensation" is a multistep process that involves epigenetic modifications of chromatin and is induced by the expression of a large non-coding RNA termed Xist. In contrast to protein-coding mRNA molecules, which are free to diffuse and roam the entire nuclear interior, Xist is locally constrained to the territory of inactive X chromosomes by as yet unclear mechanisms. Recent results have suggested a contribution of scaffold attachment factor A (SAF-A) in the silencing of X-linked genes, maybe by inducing a local change in nuclear architecture. Here, in vivo mobility experiments demonstrate that SAF-A is a component of a highly stable proteinaceous structure in the territory of inactive X chromosomes, which might act as a platform for immobilizing Xist RNA during the maintenance phase of X inactivation.