Our data revealed that HuR has the most decisive impact on the KGA/GAC protein level on a cell background that is glutamine withdraw and glutaminase-inhibition resistant (which even includes some TN tumor cells), implying that it is not the HuR levels by itself, but glutamine-dependent TCA cycle itself is the critical factor behind HuR having the most pronounced effect over KGA/GAC levels. This evidence concerns the gene ELAVL1 and neoplasm.