However, in the case of VD deficiency, the expression of gluconeogenesis-related genes G6pase and PCK1 increased in the 1,25(OH)2D3-deficient mice and HepG2 cells with VDR knockdown, demonstrating that impaired VD signaling (1α(OH)ase deletion or VDR knockdown) may increase hepatic gluconeogenesis and thus result in hyperglycaemia. The gene discussed is G6PC1; the disease is Hyperglycemia.