Three points support this hypothesis: (i) AF models with no assigned secondary structure often coincide with disordered or coil regions; (ii) a reliable portion of the N-terminal model is reminiscent of small beta barrel domains used as protein–protein interaction modules, e.g., as observed in Pleckstrin-homology domains [55]; (iii) finally, SPATA5 is thought to be a hub of protein interactions, engaging in many productive contacts [5]. This evidence concerns the gene PLEK and atrial fibrillation.