Starting from the observation that HCMV antibodies are prevalent in SSc patients [144] and that UL70 viral protein can be recognized by anti-topoisomerase I antibody, Lunardi et al. were the first to propose a novel pathogenesis mechanism of SSc based on HCMV molecular mimicry of the cellular protein NAG-2 expressed on ECs and fibroblasts, with the latter being involved in the so-called “scleroderma like phenotype” linked to SSc pathogenesis [33,83,111] (see Section 3.1 and Section 3.3). The gene discussed is TSPAN4; the disease is systemic sclerosis.