Fuzi and Ganjiang did not affect BV2 viability, ↓ TNF-α, ↓ IL-6, and ↓ ROS production, abolished iNOS-mediated NO, ↓ COX2-mediated prostaglandin E2 and ↓ NF-κB in LPS-induced BV2 microglia; in the same cells, Fuzi and Ganjiang ↑ Nrf2/HO-1 signalling pathway; low and high doses ↓ immobility in the TST, high dose ↑ open arm time in the E + M and ↓ immobility in the FST in tumour-model mice, ↓ iNOS and COX2 in PFC and Hippoc of tumour model mice with cancer-related fatigue–induced depression. The gene discussed is TNF; the disease is neoplasm.