On the other hand, at the genetic level, the accumulation of Tp53 mutation and miRNA-155 overexpression; at the molecular level, accumulation of positive feedback effects between CRS and ENKTL caused by abnormal activation of molecular signaling pathways; and at the immune level, the degree of interference of the human immune system may be the reasons for the late CA staging in some UAT-ENKTL patients with a long history of CRS. Here, TP53 is linked to congenital rubella syndrome.