Though increased expression of TGF-β and NF-κB were observed in angiotensin II-induced inflammation [18] and during heart failure [19], it is not clear if CRP also induce increased expression of NF-κB and TGF-β to promote the onset of AF following a similar pattern as being observed in the glioblastoma cells. Here, NFKB1 is linked to glioblastoma.