Allelic expression differences contribute to phenotypic variation. In X 
chromosome inactivation (XCI), unfavorable XCI ratios promote X-linked disease 
penetrance in females. During XCI, one X is randomly silenced by Xist. X 
chromosome choice is determined by asymmetric expression of Tsix whose antisense 
action represses Xist. Here, we discover a cis element in the mouse 
X-inactivation center that regulates Tsix. Xite harbors intergenic transcription 
start sites and DNaseI hypersensitive sites with allelic differences. At the 
onset of XCI, deleting Xite downregulates Tsix in cis and skews XCI ratios, 
suggesting that Xite promotes Tsix persistence on the active X. Truncating Xite 
RNA is inconsequential, indicating that Xite action does not require intact 
transcripts. We propose that allele-specific Xite action promotes Tsix asymmetry 
and generates X chromosome inequality. Therefore, Xite is a candidate for the 
Xce, the classical modifier of XCI ratios.