NFKB1 and ovarian carcinoma: Similar to CAFs and CA-MSCs, the TAMs and other immune cells in the inflammatory microenvironment can also promote ovarian CSCs through secretion of cytokines, such as IL-17, which can activate CSC promoting pathways like NF-κB and p38-mitogen activated protein kinase (MAPK), which promote CSC self-renewal and progression of ovarian cancer [70].