Further studies inferred that tumor necrosis factor-α (TNFα) and interleukin-1β (IL1β) secreted by C5aR1+ neutrophils synergistically activated the ERK1/2 signaling to phosphorylate WTAP at serine 341, thereby stabilizing WTAP, which further promotes RNA m6A modification of enolase 1 (ENO1) and leads to upregulation of ENO1, thus affecting the glycolytic activity of breast cancer cells [83]. The gene discussed is MAPK3; the disease is breast carcinoma.