A role for viral infection is further supported by the observation that molecular mimicry between human CMV late protein UL94 and NAG-2, a surface molecule present on endothelial cells and dermal fibroblasts, is responsible for cross-reactivity of human anti-CMV antibodies against the latter and may contribute to chronic sclerodermoid graft versus host disease (GVHD) [15, 16]. The gene discussed is TSPAN4; the disease is graft versus host disease.