ZMPSTE24 and Hutchinson-Gilford progeria syndrome: However, no difference was observed in H3K9me3 and/or H3K27me3/H3K27ac3 levels (Figure 6E), although altered methylation and acetylation in H3k9/H3k27 are a characteristic feature of HGPS‐derived fibroblasts and MSCs.[29] This suggests that the epigenetic markers of HGPS (representing typical progeria) and MAD (atypical progeria) do not lead to similar heterochromatin modifications.