We found that on average, 2.2 binding sites per cancer gene harbored mutations, with some tumor suppressors (FUBP1, KMT2D, NOTCH2 and MLH1) and oncogenes (CCND1 and SKP2) having no interface mutations and some cancer genes having mutations at multiple distinct interfaces (including TP53 with mutations at 8 different interfaces, CTNNB1 with mutations at 7 different interafaces, APC with mutations at 6 different interfaces and EGFR with mutations at 4 different interfaces). This evidence concerns the gene KMT2D and neoplasm.