Past research has indicated that the phosphorylation of FOXM1 at Ser25 can activate genes like IL1A/B, VEGFA, and IL6, which in turn can attract monocytes and promote the differentiation of tumor-associated macrophages (TAMs) towards an M2-like phenotype, thereby aiding in immune escape and fostering an immunosuppressive TME 60. The gene discussed is FOXM1; the disease is neoplasm.