Our results showed that short-term in vivo T3 treatment can develop cardiac hypertrophy concurrent with increased left ventricular function and associated with transient Akt activation and cyclic ERK1/2 inhibition; which implies, in close temporal proximity, activation of a physiological hypertrophy signaling and deactivation of a pathological hypertrophy signaling, respectively. The gene discussed is MAPK3; the disease is cardiac hypertrophy.