Also of note, Th2 and Th17 lymphocytes, most directly linked to IBD pathogenesis,40 were higher at baseline and reduced after DSS in octn1-/- mice compared with WT, again consistent with a preexisting expansion but reduced responsiveness of these T helper subpopulations in the context of OCTN1 deficiency. The gene discussed is SLC22A4; the disease is inflammatory bowel disease.