We found that FGA promoted GC proliferation (Fig. 2d, e) and accelerated its cycle (Fig. 2i, j) with corresponding increasing in mRNA and protein levels of PCNA, CCND1, and CCNE1. GCs are essential for follicular development, and abnormal proliferation or apoptosis of GCs leads to ovarian insufficiency [31–33]. This evidence concerns the gene FGA and ovarian dysfunction.