Whereas inhibition of TOR has been thought of as a therapeutic target in metabolic diseases that course with ER stress by decreasing ER client load and increasing insulin sensitivity (by for example, blocking TOR-mediated phosphorylation of IRS1) [51], our results demonstrate a requirement for TOR signaling in promoting ER expansion and homeostasis in eukaryotes. The gene discussed is RORC; the disease is Other metabolic disease.