JUN and progeroid syndrome: However, a subset of Ser22-phosphorylated lamin A/C-binding sites was found to be lost in progeria-patient fibroblasts but emerged in normally quiescent loci; then, new Ser22-phosphorylated lamin A/C binding was accompanied by increased histone acetylation, increased c-Jun binding, and upregulation of nearby genes implicated in progeria pathophysiology.