Nevertheless, among others, pro-survival signaling pathways such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) and mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinases 1/2 (ERK1/2) have been implicated in the cardiovascular effects of THs; importantly, in the development of cardiac hypertrophy and angiogenesis, and upholding cellular survival (3-5, 8-10) (for a schema of these pathways, see Figure 1). The gene discussed is MAPK3; the disease is cardiac hypertrophy.