As previous studies described, the increasing level of TNFA-NFκB could enhance the suppressive function of Treg cells through inducing the proliferation of Treg cells, resulting in the immune escape of tumor cells.[22,23] In addition, IL2-STAT5 could also regulate the activation of Treg cells through inducing Foxp3.[24] Besides, we found that the high risk group was also enriched in angiogenesis, TNFA-NFκB signal pathway and IL2-STAT5 signal pathway. The gene discussed is TNF; the disease is neoplasm.