Acetylation of K112 and K113 would presumably also abrogate the interaction in vivo and given that the phenotype of Scc3(D189E) and E202K mutations imply that the interaction is necessary for RA, the AF model finally provides an explanation for how acetylation would be sufficient to block RA in yeast, without any need for Sororin. The gene discussed is CDCA5; the disease is atrial fibrillation.