Our results indicate that PSELT displayed both systemic and direct anti-inflammatory actions in SHHF rats (by reducing the circulating levels of IL-1β and TNF-α) and LPS-stimulated RAW 264.7 macrophages [by reducing CD80 expression, a hallmark of M1-like proinflammatory phenotype [52, 53], suggesting that the peptide may relieve macrophage M1 activation—and the consequent release of pro-inflammatory cytokines—that closely correlate with the occurrence and progression of HF [54]. The gene discussed is IL1B; the disease is hydrops fetalis.