Taken together, the above results clearly demonstrated that mediated through LDHA, KCNK1 overexpression significantly enhanced cellular aerobic glycolysis, promoted lactate production, augmented histone lactylation, and induced the transcription of downstream targets including LDHA itself, which finally led to the proliferation, invasion, and metastasis of breast cancer cells. This evidence concerns the gene KCNK1 and breast carcinoma.