SCFAs directly suppressed pro-inflammatory cytokine production in cardiomyocytes by inhibiting the activation of NF-κB, a key transcription factor for the production of various pro-inflammatory cytokines that exacerbate adverse cardiac remodelling and contribute to heart failure.9 Indeed, NF-κB inhibition has been proposed as a promising target for treating MI.46 In addition to reducing pro-inflammatory cytokines in MI hearts, EcN_TL also up-regulated anti-inflammatory cytokines such as IL1RA and IL-10. This evidence concerns the gene NFKB1 and heart failure.