It is well established that progerin expression is associated with increased steady‐state DNA double‐strand breaks in HGPS patient cells (Constantinescu et al., 2010; Liu et al., 2006; Liu et al., 2008), in primary cells of normal human donors of advanced age (Ragnauth et al., 2010), and in cells that accumulate farnesylated prelamin A during normative aging or through related premature aging syndromes (di Masi et al., 2008; Krishnan et al., 2011; Liu et al., 2005; Liu et al., 2006; Musich & Zou, 2009). Here, LMNA is linked to premature aging syndrome.