It is predominantly pro-tumorigenic in vitro, promoting cell proliferation, migration, invasion, and resistance to apoptosis through activation of NF-κB, STAT3, ERK1/2, and EMT pathways [20,24] (see Figure 1 for a schematic representation of TNF-α signaling in the colorectal cancer microenvironment). The gene discussed is STAT3; the disease is colorectal cancer.