JunD has previously been shown to promote the proliferation of prostate cancer cells through Myc signaling [312], and inhibiting menin with either siRNA knockdown or MI-503—a menin inhibitor that blocks the menin–JunD interaction in addition to the menin–MLL interaction [313]—reduces JunD expression in AR-positive cell lines [310]. Here, KMT2A is linked to prostate carcinoma.