Importantly, the activation of NF-κB may also enhance the transcription of other pro-inflammatory factors, e.g., T cell/macrophage chemotaxis cytokine CXCL10 [34], and thereby promote the infiltration of those immune cells to the tumor microenvironment and reinforce the function of IFNγ-STAT1 and TNFα-NF-κB signaling pathways in triggering the transcription of AIM2 and PD-L1 in refractory OSCC. Here, STAT1 is linked to neoplasm.