Related to the involvement of cJUN in cardiac hypertrophy, opposing data showed that cJUN-deficient hearts of mice subjected to pressure overload displayed pronounced fibrosis and increased myocyte apoptosis, suggesting that cJUN but not cFOS is required to induce a transcriptional program aimed at adapting heart growth upon increased workload (Windak et al., 2013). The gene discussed is FOS; the disease is cardiac hypertrophy.