Also, it is unclear whether the findings from this study may be interpreted as primary or secondary events to panic disorder, although a stress-induced, and thus secondary neuroendocrinological effect of panic disorder on the immune system particularly in older females, may be a reasonable explanation for reduced thymic activity and hypermethylation of FOXP3. This interpretation is also supported by mouse models [61–64] and observations in humans [49]. This evidence concerns the gene FOXP3 and panic disorder.