Triptolide attenuates IL-6-induced activation of STAT3 target genes, such as Mcl-1 and Bcl-2, by decreasing STAT3 phosphorylation and inhibiting its nuclear translocation in NSCLC (PC9 and A549) cells, while also reversing IL-4 or LPS-induced up-regulation of IL-6 at the gene level, thereby reducing cell survival, apoptosis, and the polarization of myeloid cells into immunosuppressive macrophages and MDSCs within the tumor microenvironment [978, 979]. The gene discussed is BCL2; the disease is neoplasm.