Human endothelial cells of both vascular and not vascular soft tissues tumors were all identified by using vimentin and factor VIII antibodies. However, these molecules did not allow to know the functional state of cell activity. Nowadays, experimental and human research angiogenesis can show a heterogeneous functional response of endothelial cells explored by endoglin and SMAD regulation, KLF 6, VEGF and VEGFR. These molecules had not been quantified in cutaneous soft tissue tumours. In this report the immunochemistry and molecular expression of these endothelial epitopes in hemangiomas, dermatofibromas and lymphangiomas is evaluated, as well as in the angiogenic process found in pyogenic granuloma and granulation tissues of wound healing. 5 patients per group diagnosis of hemangioma, dermatofibromas, lymphagiomas, pyogenic granuloma and 10 patients with burned skin ulceration were examinted. The immunochemistry and molecular expression of endoglin, SMAD 1/5, SMAD 2/3, SMAD 4, KLF 6, VEGF, VEGF-R2, VEGF-R3 as well as vimentin and VIIIFG were evaluated. The evaluation of each molecule was explored using almost two slides per case. Endothelial cells in hemangiomas express VIIIFG and vimentin and no differences were found regardless of the different types of hemangiomas. The endoglin expression of hemangiomas was observed only at endothelial proliferative cells and it seems to be higher at unicellular angiotubes. Intense endoglin expression was also seen in the lumen from proliferative new vessels that showed intense endoglin expression. However, no endoglin expression was found in endothelial cells of cavernous dilation in malformative hemangiomatosis. In hemangiomas, the endothelial cell expressed SMAD 2/3 and SMAD 4, but not SMAD 1/5. Positive expression of Kruppel-like factor 6 was observed in all types of hemangiomas; but expression in proliferative endothelial cells was higher than in normal endothelial cells. Endothelial VEGF-R2 and VEGF-R3 inmunodetection was similar in hemangioma and normal vessels. Nevertheless, PCPH was found in higher concentrations in normal endothelial cells and quiescent hemangiomas, and their expression decrease in proliferative hemangiomas. In conclusion, endothelial cells in angiogenic process and vascular tumours were morphology similar, but these cells express different endothelial molecules related to distinct functional endothelial activity. Tumoral angiogenic were very heterogeneous. In hemangiomas, endoglin regulation by SMAD 2/3 and SMAD 4 indicated activation of ALK 5 that signalled pathway in these tumors.