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). This evidence concerns the gene STUB1 and infection.