In addition, intervention UCHL1 with LDN57444 led to a decrease in the percentage of dNKs in DICs (Fig. 7E, G), although the percentage of CD45+ DICs was increased in decidua from the LDN57444-treated mice (Fig. 7E, F), indicating that UCHL1 deficiency not only disrupted dNK modulation but also enhanced inflammation at the fetal-maternal interface, which collaboratively contributed to miscarriage. This evidence concerns the gene UCHL1 and spontaneous abortion.