Among urothelial carcinoma, PTEN‐PI3K‐AKT pathway was important in tumorigenesis.36 In human urothelial carcinoma, higher Akt and β‐catenin expressions were associated with higher invasiveness in urothelial cancer cells, and the deletion or mutation of p53 gene and phosphatase and tensin homolog (PTEN) activates the Akt and further tumorigenesis.37 Wu et al36 also provided the in vivo evidence that mTOR Rictor‐dependent Akt activation was an important pathway for urothelial carcinoma, and such activation could be inhibited by rapamycin. The gene discussed is TP53; the disease is urothelial carcinoma.