Among numerous disease-associated molecules, Fli1 is the only one whose expression is shown to be regulated by epigenetic and genetic mechanisms; the CpG island of the FLI1 promoter is hypermethylated in the involved skin of SSc patients, and extended repeat alleles of FLI1 (GA)n microsatellite are associated with lower FLI1 mRNA levels and susceptibility to SSc [17, 18]. This evidence concerns the gene FLI1 and systemic sclerosis.