Duan et al. reported that these mice develop cardiac hypertrophy through elevated NF-κB activity [75], and unexpectedly, rosiglitazone-induced cardiac hypertrophy in both the WT mice and cardiomyocyte-specific PPARγ knockout mice through activation of p38 MAP kinase independent of PPARγ. The gene discussed is MAPK14; the disease is cardiac hypertrophy.