HRES-1 possesses several similarities with HERV-E clone 4-1: (i) epigenetic control by DNA methylation [60]; (ii) the capacity to produce a p38gag protein that can, in turn, induce the development of Abs as observed in 52% of patients with SLE and in contrast to 3.6% in healthy donors [61]; and (iii) a cross-reactivity of the anti-p38gag HRES-1 Ab with the nuclear autoantigen U1-RNP. This evidence concerns the gene RAB4A and systemic lupus erythematosus.