LMNA and Hutchinson-Gilford progeria syndrome: For instance, dermal fibroblasts derived from patients with HGPS show changes in DNA methylation, and chromatin accessibility is enriched in NE‐associated regions, contributing to the abnormal gene expression patterns observed in HGPS.[33] Therefore, progerin accumulation leads to widespread alterations in the repressive histone mark H3K27me3, disrupting the association between heterochromatin and the nuclear lamina in HGPS fibroblasts, resulting in the loss of chromosomal compartmentalization.[34]