This protein belongs to the group of histone-modifying enzymes comprising transactivation domain 9aaTAD[6] and is involved in the epigenetic maintenance of transcriptional memory.

Rodent models of MLL1 dysfunction in forebrain neurons showed that conditional deletion results in elevated anxiety and defective cognition.

Suppression of MLL1 expression was shown to be adequate for inducing ESC-like morphology and behavior within 72 hours of treatment.

Like many other methyltransferases, the KMT2 family members exist in multisubunit nuclear complexes (human COMPASS), where other subunits also mediate the enzymatic activity.

[18] Humans with cognitive and neurodevelopmental disease often have dysregulation of H3K4 methylation in prefrontal cortex (PFC) neurons.

[19] MLL1 is required for the expression of senescence-associated secretory phenotype (SASP)-related genes and promotes increased inflammation.

[22] Despite being an aggressive leukemia, the MLL1 rearranged sub-type had the lowest mutation rates reported for any cancer.