Interestingly, Nidogen-1 (34), the heparan sulfate proteoglycan, Syndecan-4 (35), a subset of HLA-DP molecules (36), a splice variant of the MLL5 gene (37), and PCNA (38), have all been reported to bind and regulate NKp44 signaling, and it will be interesting to determine whether expression of these latter genes in the LGG tumor microenvironment can influence the association between the NK cell phenotypes that we describe and LGG prognosis. The gene discussed is KMT2E; the disease is neoplasm.