NLRP3 and Yersinia infectious disease: Loss of TAK1 leads to the spontaneous activation of NLRP3 in a RIPK1-dependent manner, leading to the subsequent induction of cell death.147 Further studies have found that TAK1 inhibition after Yersinia infection leads to the CASP8-dependent cleavage of GSDMD and GSDME in a RIPK1-dependent manner.148–150 While there are still many unanswered questions regarding TAK1-mediated regulation of NLRP3 and cell death, these and other studies help to highlight the complexity of communication between cell death pathways.