This mutual amplification mirrors feedback loops observed in other cancers, such as the NAT10/SEPT9/HIF-1α axis in gastric cancer glycolysis [18] and the NAT10/KIF23/GSK-3β axis in colorectal cancer progression [31], underscoring the critical role of NAT10 in sustaining oncogenic signaling networks. This evidence concerns the gene HIF1A and colorectal cancer.