Underscoring a potentially essential tumor suppressor role for KMT2D, recent work has shown that KMT2D is critical for the promotion of epidermal differentiation through its interaction with the master epithelial transcription factor, p63 [71], as well as through its ability to promote tumor suppressive ferroptosis, a form of iron-dependent programmed cell death [72,73] (Figure 2). Here, KMT2D is linked to neoplasm.