It may also be stored in the endoplasmic reticulum or Golgi apparatus.[195] Cobalt disrupts iron–sulfur clusters, leading to oxidative stress and necessitating the upregulation of genes involved in Fe‐S cluster biosynthesis and cobalt efflux.[196] The ferroportin (FPN) metal efflux proteins also play a role in cobalt homeostasis in mammalian systems and thus influence both the iron deficiency response and sensitivity to cobalt.[197]. The gene discussed is SLC40A1; the disease is nutritional disorder.