One possible explanation for the duration of THECs activation independent of TS stimulation is that initially activated regenerative signals could be efficiently maintained and transmitted, akin to the inflammatory cascade observed during injury recovery, sepsis, and infections.[44] While the positive feedback loop between YAP/TAZ and Notch1/Dll4 signaling provides a biological basis for synergistically activating tissue regeneration signals, intercellular communication of regenerative signals within the microenvironment is also crucial. The gene discussed is DLL4; the disease is infection.