However, we posit that HFD-induced neuroinflammation uniquely promotes insulin resistance within the NAc as a primary driver of reduced reward value that promotes overconsumption of palatable foods, but a major gap involves lack of pharmacological investigation assessing interactions between insulin, LPS, inflammatory cytokines and microglial activation on behaviour and presynaptic dopamine neurotransmission in the NAc after chronic HFD intake during obesity. The gene discussed is INS; the disease is obesity disorder.