This molecular signaling system is a candidate contributor to the studies mentioned above in which thyroid hormone induced myocardial hypertrophy [1] and one can speculate that amplification of STAT3 action by thyroid hormone-directed ERK1/2 might be the vehicle by which thyroid hormone can enhance angiogenesis whether or not cardiac hypertrophy is present. The gene discussed is STAT3; the disease is cardiac hypertrophy.