Although it has been established that the presence of lymphocytes is necessary and increase in vascular adhesion molecules and cytokines are required for lymphocyte accumulation at a certain site, there is a supporting hypothesis indicating that the main mechanism for lichen planus is lymphocyte activation by increasing vascular adhesion factors, such as ELAM1, VCAM1, ICAM1, and lymphocytic infiltration through increase in L-selectin, LFA-1 and VLA4 receptors (7). The gene discussed is ICAM1; the disease is lichen planus.