Collectively, MLL1 loss-of-function effects on SAP30-mediated breast tumor growth and metastasis were supported by the in vitro and in vivo results from MLL1 binding–resistant SAP30 F186E/F200E mutant (Figure 5, A–H), and thus these combined results indicate that SAP30-mediated breast cancer progression is MLL1 dependent. This evidence concerns the gene KMT2A and breast carcinoma.