We found that IL1R downstream signaling molecules including NF-κB/MAPK signal transducers were highly up-regulated thereby enabling MCF10A-SNAI1 cells to respond dramatically to exogenous IL1ß, producing high amounts of IL6 and IL8. Recently, the pivotal role of IL1ß, IL6, and IL8 in CSC formation has been identified, supporting the links between inflammatory states and cancer development [30]. The gene discussed is NFKB1; the disease is cancer.