Another hypothesis based on this assumption is that because elevated serum TSH levels are reversible after weight loss, this may not be ‘true’ subclinical hypothyroidism and may possibly be a result of adaptive responses to thyrotropic feedback control i.e. obesity leading to increase in serum leptin-mediated Pro TRH [17–19] and increase in resting energy expenditure [10, 16] which in turn, leads to a higher serum TSH level. The gene discussed is TRH; the disease is Obesity.