Aside from these common pathways, there might be two other distinct mechanisms to clarify the association between fibrinogen and outcomes of XP11.2 translocation RCC, a tumor which has been demonstrated to involve VEGF and mTOR pathways [11, 12]: as an extracellular matrix element, fibrinogen could regulate growth of cancer cells by binding to VEGF [22]; alternatively, fibrinogen may promote cell motility by inducing epithelial-mesenchymal transition via the p-AKT/p-mTOR pathway [23]. Here, AKT1 is linked to neoplasm.