IL-18 activates PI3K via its receptor and the downstream MyD88/IRAK1/TRAF6 complex, subsequently promoting the expression of ECM components such as FN through the AKT–IKKβ–NF-κB pathway, thus participating in myocardial fibrosis (Reddy et al., 2008). Here, PIK3CB is linked to Myocardial fibrosis.