The lymphatic vessels (LV) form a network parallel to the blood vessels and drain the fluids, molecules and cells of the extracellular compartment of the tissues. They also have a very important function in innate and adaptive immunity. In tumor context, lymphatic endothelial cells (LEC) forming LVs proliferate through a process of lymphangiogenesis induced by tumor microenvironment (TME) factors which promote the development and spread of metastases while facilitating the initiation of the response. immune anti-tumor. A promising strategy in cancer research is immunotherapy, but the ability of tumors to evade the immune system complicates the development of effective therapies. LECs do not just drain immune cells, they actively act on their recruitment and activity, so understanding the mechanisms associated with the functions of tumor LECs is very important. We have shown that TME modifies a number of genes in tumor LECs. By taking a closer look at IFNγR we have demonstrate that its expression is up-regulated in B16F10 OVA+ VC+ melanoma-associated LECs compared to dermal LECs. The use of a transgenic mice model overexpressing IFNγR selectively in LECs has revealed that an increase in sensitivity of LECs to IFNγ tends to decrease the development of the primary tumor such as metastases. These consequences could be caused by an IFN-γ dependent inhibition of tumor-associated lymphatic density observed in this model.