Although the up-regulation trend of p53 expression is not as significant as p-p53, which may be due to different biological genetic backgrounds of different cell lines, given that p-p53(SER15) has a obvious pro-apoptotic effect on tumor cells47-49, these results have already revealed that anlotinib inhibited the DNA damage response and induced p53-dependent apoptosis in tFL cells by destroying SETD1A, suggesting the potential value of anlotinib in tFL. This evidence concerns the gene SETD1A and neoplasm.