Thus, our study could show that the reduced levels of intracellular lipids in both the pretreated and concurrently treated HepG2 cells and primary rat hepatocytes with SKK were through the modulation of the FFA-stimulated steatosis related transcription factors (SREBP1c and C/EBPα), and associated lipogenic gene (FAS), which in turn also normalized the fatty acid transporter (CPT1A) gene expression levels responsible for the transport of fatty acids for mitochondrial energy metabolism. The gene discussed is FAS; the disease is steatosis.