Loss of KMT2D impacts glycolysis pathways, making lung cancer cells more vulnerable to glycolytic inhibitors,34 and also leads to increased activity of receptor TKs such as EGFR and ERBB2/HER2.35 By contrast, our analysis highlights extensive epigenetic modifications associated with KMT2D mutations, particularly affecting histone methylation at H3K4, H3K9 and H3K27. This evidence concerns the gene EGFR and lung carcinoma.