Those observations have led to the hypothesis that Prelamin A and/or Progerin sequesters PCNA, as evidenced by the diminution of MCM7-PCNA interaction in HGPS cells [339] or by the increased PCNA monoubiquitination and the increased colocalization of POLη and PCNA foci with γH2AX after Prelamin A ectopic expression [336]. The gene discussed is LMNA; the disease is Hutchinson-Gilford progeria syndrome.