Recently, dermal ECs explanted from KLF5+/−; Fli1+/− mice, a new animal model resembling the fundamental pathologic features of SSc, were reported not only to be defective in performing in vitro angiogenesis, but also to have a reduced expression of VE-cadherin and CD31, suggesting the occurrence of EndoMT, as observed in SSc-affected ECs, and highlighting that a deficiency of KLF5 transcription factor may be another important trigger of this process [59]. Here, FLI1 is linked to systemic sclerosis.