Tamoxifen-inducible global knockout of FAS results in a preferential decrease in ether-linked glycerophosphocholines (ether-lipid equivalent of phosphatidylcholine; GPC) in neutrophils (Lodhi et al., 2015), increased ER stress and apoptosis, resulting in nearly complete neutropenia, suggesting that FAS channels fatty acids to peroxisomes for lipid synthesis. The gene discussed is FAS; the disease is Decreased total neutrophil count.