Consistent with the hypothesis that Ser22-phosphorylated Lamin C acts as a transcriptional activator, gains of Ser22-phosphorylated Lamin C binding were correlated with acquisition of histone acetylation and c-Jun binding at the binding sites, and losses with reduction of histone acetylation and c-Jun binding in progeria-patient cells [28]. Here, JUN is linked to progeroid syndrome.