Moreover, lymphotoxin and LIGHT can engage LTβR on stromal components of TME, such as fibroblasts and endothelial cells promoting the secretion of chemokines and contributing to endothelial cell activation, accompanied by increased expression of adhesion molecules, resulting at the end in the recruitment of effector cells and the subsequent control of tumor growth [37, 50, 55]. This evidence concerns the gene TNFSF14 and neoplasm.