The main finding of this study is that sildenafil in human cardiomyocytes inhibited protein and gene expression of IFNγ + TNFα-induced chemokine CXCL10 (IC50 2.6 × 10−7 M), which is a critical trigger of early Th1 immune/inflammatory response during cardiac diseases [12–17]. The gene discussed is CXCL10; the disease is heart disorder.