Fig. 3
From: Emerging roles of H3K9me3, SETDB1 and SETDB2 in therapy-induced cellular reprogramming
A hypothetical mechanisms for type I IFN-mediated induction of SETDB1 and SETDB2 by STAT1 and Wnt5a respectively. Feedback attenuation proposed through inhibition of pro-IFN signalling cytokines and KAP1-SETDB1 interactions. Key at bottom