Mechanistically, FCGR2A activation in tumor-associated macrophages triggers SYK-dependent PI3K phosphorylation (p-PI3K[Y607]↑2.8-fold vs controls, p=0.004), which subsequently enhances AKT-mediated lipid metabolic reprogramming through SREBP1 activation (mRNA↑3.1-fold, p=0.009) (78). The gene discussed is AKT1; the disease is neoplasm.