In later AD stages characterised by the spreading of NFT and neuroinflammation, CSF1R inhibitors could prevalently act by decreasing the number of microglia with a pro-inflammatory phenotype, whereas GM-CSF might exert favourable effects by their immunomodulatory action as suggested by sargramostim-induced increase in the levels of both inflammatory (IL-6 and TNF-α) as well as ant-inflammatory (Il-10) cytokines, observed in patients with mild to moderate AD (Potter et al., 2021). The gene discussed is CSF1R; the disease is Alzheimer disease.