In human HepG2 cells, PXR activation by rifampicin promoted steatosis via induction of SREBP-1 pathway (mainly SREBP-1a), whereas PXR silencing enhanced AKR1B10 expression, which subsequently stabilized the acetyl-CoA carboxylase, thereby promoting de novo lipogenesis [10]. The gene discussed is NR1I2; the disease is steatosis.