APOA1 and atherosclerosis: Furthermore, anti-ApoA1-IgG induces atherosclerosis in a TLR2/TLR4/CD14-dependent manner through two pathways: it guides the expression of inflammatory factors by activating transcriptional nuclear factor-kappa B (NF-κB); it provides an alternative (or concomitant) signal to phosphoinositide 3-kinase (PI3K) in an Src-dependent pathway, activating L-type Ca2+ channels and potassium/calcium exchangers, resulting in the depolarization of myocardial plasma membrane [38].