As given in Figure 6A, in maintained COS-7 cells expressing multiple vectors, including empty pCI as an external negative control (−), wild-type human SOX4-pCI (SOX4), and Gln71*-mutant human SOX4-pCI (Gln71*), singly or in combination, SOX4 (simulating the physiological state of a healthy person) and Gln71* (simulating the pathological condition of an AF patient with a homozygous SOX4 mutation of Gln71*) transactivated the GJA1 promoter by ~11-fold and ~1-fold, respectively (SOX4 versus Gln71*: t = 12.4897; p = 0.0002). This evidence concerns the gene SOX4 and atrial fibrillation.