Conversely, adenovirus-mediated overexpression of SOCS3 in cardiomyocytes markedly inhibits the LIF and CT-1-induced hypertrophic response, as well as activation of gp130 downstream signals (Yasukawa et al., 2001), suggesting that SOCS3 may be a new potential therapeutic target for treatment of cardiac hypertrophy and HF. The gene discussed is SOCS3; the disease is hydrops fetalis.