At the tumor-cell level, LPS–TLR4 signaling drives migration/invasion via a METTL3–PI3K/AKT axis—an effect attenuated by pharmacologic or genetic interference—and translationally nominates companion measurements and a druggable node for combination with checkpoint blockade or myeloid-reprogramming [164, 165]. This evidence concerns the gene AKT1 and neoplasm.