In silico predictions suggested that they were involved in several important biological processes and functional pathways associated with AF, such as TGF-beta 1 and Insulin-like growth factor 1 (IGF-1) signaling, proliferation and cellular adhesion (MAPkinase and AKT pathways), and circadian clock/synchronisation of circadian rhythmicity, but also in RNA-mediated gene silencing (i. e. AGO/EIF2C proteins) and miRNA machinery (i. e. TNRC6 proteins), further suggesting that alteration of miRNAs in LA would in fact perturbate the whole miRNome. The gene discussed is CLOCK; the disease is atrial fibrillation.