By the genetic ablation of KMT2A (CRISPR/Cas9), as well as mutations of the SET domain or the pharmacological inhibition of important protein–protein interactions of the KMT2A complex, it was shown that the H3K4me3 mark was reduced in tumor cells, and the sizes of tumor organoids and tumor spheres were greatly diminished [153]. Here, KMT2A is linked to neoplasm.