Normally, HuR is located in the nuclei, however, stimuli (e.g., hypoxia, glucose deprivation, chemotherapy) in the tumor microenvironment will cause HuR relocation from the nucleus to the cytoplasm and promote HuR to bind to U- or AU-rich sequences in the 3′UTR of target mRNAs which confer cellular responses including cell growth, apoptosis and cell cycle [23]. This evidence concerns the gene ELAVL1 and neoplasm.