In addition, the antiapoptotic B-cell lymphoma-extra large (Bcl-xL) protein prolongs the lifespan of protumorigenic TANs via JAK/STAT signaling, with tumor cell-derived GM-CSF triggering the expression of Bcl-xL.35 In a mouse model, the use of the Bcl-xL inhibitor A-1331852 selectively can reduce the abundance of protumor TANs, replacing them with antitumor TANs, with the administration of G-CSF counteracted neutropenia in patients.35 Therefore, targeting alternative pathways that selectively inhibit N2 TANs also represents a promising direction for future cancer therapies. Here, CSF3 is linked to neoplasm.