It has been previously shown that MK2 limits RIPK1 activation by phosphorylating it at S320/S335 residues (S321/336 in murine RIPK1) in response to pro-inflammatory stimuli such as TNF, LPS and Yersinia infection, and therefore, can control RIPK1-dependent cell death [14–16]. Here, TNF is linked to Yersinia infectious disease.