The AT-rich interactive domain 1A gene (ARID1A) and the phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit α gene (PIK3CA) are frequently mutated in OCCC, and co-mutation in transgenic mice promotes OCCC tumor initiation, possibly by continuous stimulation of interleukin-6 (IL-6)-dependent pro-inflammatory and pro-tumorigenic signaling as IL-6 is elevated in OCCC patients4. Here, IL6 is linked to neoplasm.