Previous studies demonstrate that PRMT5 activity is essential for cell stemness.7, 38, 39 In breast cancers specifically, PRMT5 was shown to play a critical role in the proliferation and self‐renewal of stem‐like cells via the regulation of C‐MYC, OCT4/A, and FOXP1 expression.7, 38, 39 Our study supports these findings as we show that PRMT5 inhibition impairs the formation of mammospheres—an indicator of cancer cell stemness—in a TNBC cell line. Here, FOXP1 is linked to breast cancer.