Importantly, deficiency of NLRP3 or Caspase-1 significantly blocked the OT1 CTL-mediated rejection of EG7 tumours (Fig. 5c,d).Consistently, we found that IL-1β secretion was blocked in Nlrp3-, Caspase-1- and β2M-deficient mice (Fig. 5e), indicating that antigen-specific activation of NLRP3 inflammasome is required for IL-1β maturation in the CTL-mediated tumour rejection model. Here, B2M is linked to neoplasm.