Additionally, I3AA antagonizes AhR signaling, a pathway essential for maintaining gut immune homeostasis, further exacerbating immune dysregulation.[21] In contrast, Blastocystis ST4 colonization has been associated with an anti‐inflammatory immune profile, characterized by enhanced Treg differentiation and suppression of Th17 cells expressing IL‐17A in an experimentally induced colitis model. The gene discussed is IL17A; the disease is colitis.