CTGF, a key mediator of fibrosis in pathological cardiac hypertrophy [28], is negatively regulated by KLF15 and increased TGFβ levels activate p38-MAPK signaling which downregulates KLF15 leading myocardin to bind to SRF and to activation of cardiotrophic genes [15]. Here, KLF15 is linked to cardiac hypertrophy.