The finding that CHIP is a cardiovascular risk factor, increases the propensity to certain types of infection, and that Tet2 dysfunction leads to sub-optimal emergency myelopoiesis (273), means investigating whether CHIP has a role in NLRP3 hyperactivation, peri-operative and ICU-acquired non-ischaemic myocardial injuries, the inability to resolve inflammation is a high priority particularly as it may be important targetable driver of hyperinflammation in both the acute and survivor phases of critical illnesses (288). The gene discussed is NLRP3; the disease is infection.