Disrupted nuclear lamina was observed in p.R527C derived cells without the accumulation of pre‐lamin‐A protein, despite the accumulation of progerin or pre‐lamin‐A being considered a common attribute of HGPS and MAD disorders, respectively.[41] This suggests that heterochromatin modification due to disrupted nuclear lamina can occur independently of pre‐lamin‐A. This evidence concerns the gene LMNA and Hutchinson-Gilford progeria syndrome.