A recent study indicated that the AKT/mTOR signaling pathway could be directly activated by PD-1/PD-L1 during the malignant progression of DLBCL.[36] Similarly, TP63 also could regulate mTOR signaling, which play a critical role in the progress of DNA damage.[37] Our previous study showed that PD-L1 dysfunction could promote the progression of leukemia via regulating JNK/cyclin D2 signaling.[38] Thus, we speculated that PD-L1/TP63's overexpression may activate some important intracellular signaling results in tumor development, which need more further studies to elucidate. This evidence concerns the gene CCND2 and neoplasm.