
-   Slfn4 seems to play a role in lung alveolarization. Slfn4 mRNA expression peaked on fetal day 21, decreased 2- to 3-fold during alveolar septation, and then increased again 3-fold after alveolar septation. Moreover, Slfn4 expression as increased in animal models of arrested alveolarization [PMID: 17911382].
-   The myeloid differentiation factor Schlafen4 (Slfn4) marks a subset of myeloid-derived suppressor cells (MDSCs) in the stomach during Helicobacter-induced spasmolytic polypeptide-expressing metaplasia (SPEM) [PMID: 31980446]. Gli1 deletion prevents Helicobacter-induced gastric metaplasia. Use of microarray analysis to identify GLI1 target genes showed that induction of Schlafen-4 contributed to the GLI1-dependent development of mucous neck cell metaplasia [PMID: 23520544].
-   Slfn4 mRNA levels were up-regulated during macrophage activation but down-regulated during differentiation. Constitutive *Slfn4* expression in the myeloid lineage *in vivo* perturbs myelopoiesis [PMID: 21249125].
-   Slfn4 deficiency improves MAPK-mediated inflammation, oxidative stress, apoptosis and abates atherosclerosis progression in apolipoprotein E-deficient mice [PMID: 34757313].
-   In a mouse collagen-induced arthritis (CIA) model of rheumatoid arthritis, Slfn4 mRNA expression increased ~8 fold compared to joints that were not disease-affected. This data shows the induction of Slfn4 gene in macrophages to inflammatory processes [PMID: 21249125].
