Several studies have reported that activation of IL‐17 signaling can promote macrophage recruitment,[17] polarize macrophages toward a proinflammatory transcriptome,[18] or even enhance the expression of TLR4 in macrophages.[19] By using scRNA‐seq, our study firstly demonstrated the activation of IL‐17 signaling in TLR4‐dependent proinflammatory macrophage subsets at early stage of experimental anti‐GBM cGN, indicating the IL‐17 mediated downstream cascade may be another potential mechanism in anti‐GBM cGN. The gene discussed is CGN; the disease is glioblastoma.