Clinical syndromes of hormone resistance or independence have baffled clinicians 
for decades. These syndromes sometimes result from mutations or deficiencies in 
enzymes that activate prohormones or from alterations in signal transduction 
proteins. The majority of these conditions, however, arise from abnormalities of 
hormone receptors. We describe examples of syndromes that result from genetic 
mutations or misexpression of steroid/thyroid hormone receptors, with a specific 
emphasis on thyroid and androgen resistance syndromes, and estrogen independence 
in breast cancer.