Targeting NOX4 in murine models of CAF rich tumours (either by silencing or pharmacologically inhibition) suppressed the TGF-β mediated differentiation into myofibroblasts and additionally downregulated functional markers including αSMA and collagen 1 of fully differentiated CAFs resulting in a more “quiescent” state and a rescued CD8+ TIL response by redistribution of CD8+ T cells into the tumour (33). Here, ACTA1 is linked to neoplasm.