As shown in Fig. 2, in cancer patients the interaction between G‐CSF/GM‐CSF and G‐CSFR/GM‐CSFR could cause receptor dimerization, tyrosine phosphorylation, and the subsequent interaction with multiple intracellular signaling pathways such as Ras, MAPK, PI3K, JAK [58], finally inhibiting normal differentiation of HSCs and inducing the production of tumor‐promoting cell phenotypes [59]. The gene discussed is CSF3; the disease is cancer.