SRC-2 works as crucial integrator of circadian behavior governed by light and metabolic homeostasis sustained by the liver; notably, a lack of SRC-2 causes mice to be unable to adapt to the stress of chronic circadian disruption and provokes NASH and HCC gene signatures [90], demonstrating the fundamental role of circadian cycles in the development of HCC. This evidence concerns the gene NCOA2 and metabolic dysfunction-associated steatohepatitis.