AKT1 and cardiac hypertrophy: Previous studies have found that IL-18 induces expression of NF-κB [24], which impairs cardiac function, and was dependent on myeloid differentiation 88 (MyD88) → interleukin 1 receptor (IL-1R) associated kinase (IRAK) → TNF receptor-associated factor 6 (TRAF6) → PI3K → Akt → induced IκB kinase (IKK) → NF-κB inducing the expression of fibronectin [3, 4, 21], and further mediated myocardial hypertrophy.