For instance, fibroblasts from HGPS patients exhibit abnormal nuclear morphology associated with loss of heterochromatin markers H3K9me3, HP1α, and HDAC1; also, the presence of progerin in these cells has been associated to impairment of several pathways, including canonical Wnt/β-catenin and TGF-β signaling, and gene expression (Andres and Gonzalez, 2009; Maraldi et al., 2011). Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.