In this work, using MSCs isolated from bone marrow of SSc patients, which are largely accepted as an alternative source of functional pericytes[11-15,18], we provide evidence that these cells display a failure in Cav-1 trafficking inside the cell, which lead to a significant decrease of VEGFR2 proteosomal degradation, upregulation of the VEGF downstream pathways, and finally, a consequent increased expression of CTGF. The gene discussed is CAV1; the disease is systemic sclerosis.