The previous study had shown that STK11 mutations in lung cancer lead to a “cold” tumor immune microenvironment (TME).37 Functional loss of STK11 can disrupt the lactate transporter MCT4, increasing lactate production and export in the tumor microenvironment; excess lactate promotes macrophage polarization to the M2 phenotype, reducing T-cell infiltration and function, which can contribute to immune escape.38 Taken together, this suggests neoadjuvant immunochemotherapy in cervical cancer may be more reliant on changes in the characteristics of the TME. This evidence concerns the gene STK11 and cervical carcinoma.