Taken together in the context of findings referenced in this review, these observations may suggest a fulcrum in TAM activation status at some point between the intermediate and late time points, whereafter glioma cells are able to tip the balance toward an alternatively activated M2 TAM phenotype, thereby amplifying autocrine and paracrine loops successful in recruiting greater numbers of TAMs which do not express TNF-α. The gene discussed is TNF; the disease is central nervous system cancer.