It has been reported that SEPT9 upregulates HIF‐1α by blocking RACK1 activity in prostate cancer.[42] Increased expression of HIF‐1α can activate the transcription of HK and PDK, which further initiates glucose metabolism reprogramming.[43] Therefore, NAT10 might upregulate SEPT9 expression through mRNA ac4C modification and form a NAT10/SEPT9/HIF‐1α positive feedback loop that constantly over‐activates transcription of glycolytic enzymes downstream of the HIF‐1 pathway, consequently promoting glycolysis addiction of GC cells in a hypoxic microenvironment. Here, SEPTIN9 is linked to prostate carcinoma.