I have had a strong and longstanding interest in hepatic and mitochondrial metabolism under hormonal control and drug toxicity. My recent research work currently is focused on understanding the hepatic actions of nuclear hormone receptors such as thyroid hormone receptors (THRs) and estrogen related receptors (ERRs). In particular, I have found that thyroid hormone (TH) together with ERRalpha, regulates mitochondrial biogenesis, fission, mitophagy and other key mitochondrial processes (Sci Signal, 2018; Nat Rev Endocrinol, 2018) that are important for mitochondria homeostasis and cell health, and may have implications in metabolic diseases and aging. I previously demonstrated that TH activation of SIRT1 leads to inhibition of MTORC2-AKT signaling that increases nuclear localization of FOXO1 and its activation via SIRT1-mediated deacetylation. This novel mechanism showed that nuclear hormone receptors could directly activate other transcription factors and their target genes through SIRT1 (J Biol Chem, 2016 and 2013; Trends Endocrinol Metab, 2014). Given the large repertoire of protein targets that can be deacetylated by SIRT1, we embarked on acetylome studies to identify proteins that may be regulated by SIRT1 deacetylation. In our preliminary work in human hepatic cells, we identified about a dozen proteins that are deacetylated by SIRT1 in the liver, and FASN appears to be the most promising with respect to metabolism and non-alcoholic fatty liver disease (NAFLD) given its prominent role in fatty acid biosynthesis. On the other note, we also showed how nuclear hormone activates mitochondrial quality control by autophagy, a novel regulation of nuclear hormone action, to regulate energy metabolism (Autophagy, 2015 and 2018; Endocr Rev, 2016).