Furthermore, loss/redistribution of Cx40 appears to be a common feature of other murine models of AF including overexpression of RHOA, overexpression of constitutively active RAC1, cardiac-specific overexpression of ACE, overexpression of Tumor necrosis factor (TNF), and cardiac overexpression of cAMP Response element modulator (CREM; Sah et al., 1999; Kasi et al., 2007; Sawaya et al., 2007; Adam et al., 2010; Kirchhof et al., 2011a; see Table 1 and Figure 1 for further details). This evidence concerns the gene RHOA and atrial fibrillation.