Second, we show how the model explains (i) delays and hysteresis, (ii) the ability of the HPT axis to compensate for physiological changes by means of gland‐mass growth and shrinkage, (iii) the transition between subclinical and clinical states of Hashimoto's and Graves' diseases, and (iv) the three‐regime TSH/T4 relationship. The gene discussed is CD4; the disease is Graves disease.