NFKB1 and neoplasm: IL-17 could stimulate tumor proliferation and self-renewal and promote tumor infiltration and angiogenesis by activating downstream transcription factors (STAT, NF-κB, and AP1), antiapoptotic proteins (mTOR, Akt, Bcl-2, Erk, and Bax), and kinases (MAPK and HER1) [36, 37].