Furthermore, metabolism of PC species has been linked to NASH pathogenesis: hepatic deletion of phosphocholine cytidylyltransferase (PCYT1) and knockdown of LPCAT3, two enzymes involved in PC metabolism, results in marked reductions in VLDL secretion, a key factor in the development of NASH in humans [15]. The gene discussed is PCYT1A; the disease is metabolic dysfunction-associated steatohepatitis.