Numerous cell‐stress signalling pathways are frequently initiated by acute cell/organ damage with the aim of cell proliferation/cell survival and death.35 In the present study, we found that several cell‐stress signalling pathways, including PI3K/Akt/m‐TORAkt substrates (FoxO1/GSK3β), p90RSK (ie MAPK‐activated protein kinase‐1 for regulating CREB), p‐ERK1/2 and p‐PKC, were activated in CKD animals, suggesting intrinsic responses for ischaemia/stress stimulation. The gene discussed is CREB1; the disease is chronic kidney disease.