Using several ectopic and orthotopic mouse tumor models, Frindleder et al. demonstrated that blocking of the TGF-β signaling, accomplished via neutralization of the cytokine itself either via inhibition of its receptor (TGFβR) or via inhibition of the intracellular kinases involved in downstream signaling, resulted in recruitment and activation of CD8 + T cells, macrophages and a TAN phenotype with significant cytotoxic antitumor properties, characterized by the expression of CD101 and CD177 surface markers [37]. Here, TGFB1 is linked to neoplasm.