Previously, activation of p53 was associated with tubular apoptosis in cisplatin‐induced injury in mice.8 It was also shown that cisplatin‐induced activation of ERK p38 and JNK/SAPK in vivo preceded the development of AKI.9 Phosphorylation of p38‐MAPK and NF‐κB was found to be up‐regulated in rat kidneys following gentamicin treatment.10 In our cisplatin‐induced model, the number of dysregulated phosphoproteins decreased over time (day 28) and was mostly represented by proteins involved in cell growth and proliferation. The gene discussed is MAPK8; the disease is acute kidney injury.