This observation is particularly relevant to the understanding of pathological accumulation of farnesylated prelamin A. Previous studies have shown impaired 53BP1 recruitment to DNA damage foci in the presence of L647R-prelamin A (uncleavable farnesylated prelamin A (Cobb et al., 2016) and other progeria-linked prelamin A forms (Starke et al., 2013) including progerin, the truncated form of farnesylated prelamin A accumulated in HGPS (Starke et al., 2013; Kreienkamp et al., 2016). This evidence concerns the gene TP53BP1 and progeroid syndrome.