Anti-cell proliferation, a critical effect of MA, was shown on leiomyoma cells by targeting sterol o-acyltransferases (SOATs), blocking cholesterol esterification and the accumulation of free cholesterol, which induced unfolded protein response (UPR) sensors, PRK-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme (IRE1), and activating transcription factor (ATF6), leading to endoplasmic reticulum (ER) stress-induced cell death (Lin et al., 2023). This evidence concerns the gene EIF2AK3 and leiomyoma.