On the other hand, the stable expression of markers associated with gut homing or inflamed tissues (integrin α4β7, CCR9, and CXCR3) (Figures 2 and 3), indicates that blocking such molecules may be successful when treating CeD over longer period of time.[12] Nonetheless, it is possible that similarly dynamic shifts in phenotypic features of pathogenic T cells will play out in other autoimmune conditions as well, especially those including flares or other fluctuating courses of disease activity. Here, CCR9 is linked to cranioectodermal dysplasia.