We adopted the HL-1 cell line—the model cardiac cell with functional properties comparable to the normal cardiomyocytes, to determine (1) the effect of CRP on the proliferation and apoptosis of HL-1 cells; (2) the effect of CRP on the secretion of pro-inflammatory factor IL-6 hallmarked in AF; and (3) the role of NF-κB in TGF-β/Smad signaling upon CRP treatment. This evidence concerns the gene NFKB1 and atrial fibrillation.