For example,IL-1β, IFN-γ, or TLR signals can upregulate MHC-II and immune modulators in MKs, promotingan MK1-like phenotype [57], whereas IL-6 or TGF-βfavors platelet-generating MK2-like features [58].The inflammatory phase may further influence MK subset dynamics: MK2 predominates duringacute infection, supporting coagulation and neutrophil activation, whereas MK1 becomes moreprominent during chronic or recovery stages to mediate immune regulation—consistent with ourfindings in PICS and sepsis. The gene discussed is IL1B; the disease is infection.