We provide a pathway model of the NLRP3-inflammasome after cellular damage. NLRP3-inflammasome attenuation by paracrine IFN-I is more potent than by IFN-II. Change from IFN-II to IFN-I may stop inflammation during tissue repair after infarct. Impairment of IFN-I feedback can lead to hyperinflammation as in spontaneous colitis. Regulation of inflammation may directly be encoded within regulatory pathways.