This CpG site with reduced methylation levels in AD patients was at the proximal upstream of the Th2-specific DNA hypersensitive site in the IL13 promoter but within the Th2 locus-control long non-coding RNA37 (Fig. 2d), indicating that this epigenetic modification might functionally explain the augmented capability of CD4+CLA+ T cells of AD patients to produce IL-13. Here, IL13 is linked to Alzheimer disease.