CD8A and neoplasm: However, this was not associated with reduced CAF levels or reduced CD8 T cells at the tumour margin, indicating a CAF- and exclusion-independent mechanism.3 In support of this, in vitro analysis showed that TGF-β1 inhibition prevents CAF activation, but does not reverse the established CAF phenotype.3 NOX4 is known to act downstream of TGF-β1, and its inhibition was sufficient to reverse CAF differentiaion and ‘normalise’ the cell, suggesting that investigating downstream mediators of TGF-β1 signalling could lead to further identification of novel therapeutic targets.