In the current human research, the Gln71* and Trp97* mutations in SOX4 uncovered in patients affected with AF were predicted to produce truncated SOX4 proteins losing TAD along with about halves of the HMG domains, hence anticipated to fail to bind target DNA and activate transcription, and quantitative biochemical measurements demonstrated that Gln71*- or Trp97*-mutant SOX4 failed to transactivate the expression of GJA1 as well as SCN5A in synergy with TBX5. This evidence concerns the gene SOX4 and atrial fibrillation.