Supporting evidence suggesting the contribution of Th17 cells and pro‐inflammatory IL‐17 to AITD, particularly HT, has been produced in the last decade.3, 4, 5, 6 It has been proposed that AITD results from Th1/Th2 dichotomy and Th17/T regulatory (Treg) cell imbalances.7 The gene discussed is IL17A; the disease is hematocrit.