Several putative molecular mechanisms may be involved in A-type lamins alterations including mutations in the LMNA gene [20], epigenetic LMNA promoter modifications [31], degradation induced by viral infection (either HPV or HIV) [29], or impaired activity of a protease (ZMPSTE24) involved in the maturation of prelamin A into functional lamin A [32, 33]. The gene discussed is ZMPSTE24; the disease is viral infectious disease.