as shown by liu et al., lack of zmpste24 prevents lamin a formation from its precursor farnesyl-prelamin a. lack of zmpste24 causes progeroid phenotypes in mice and humans. this lack increases dna damage and chromosome aberrations and sensitivity to dna-damaging agents that cause double-strand breaks. also, lack of zmpste24 allows an increase in non-homologous end joining, but a deficiency in steps leading to homologous recombinational dna repair.