SMARCA4 and metabolic dysfunction-associated steatohepatitis: We have previously reported that hepatocyte conditional BRG1 knockout (LKO) mice exhibited deceleration of ROS accumulation in the liver compared to the WT littermates in a model of non‐alcoholic steatohepatitis.[13] In the present study we have identified DDIT4 as a novel target for BRG1, which undergoes cysteine S‐nitrosylation and scaffolds the p38 signaling complex to promote ROS‐induced liver injury.