In conclusion, the regulation of BTG2 by SETD1A serves as a model to illustrate (1) the exquisite target specificity exhibited by histone lysine methyltransferases, (2) a miRNA network-mediated mechanism through which SETD1A, a positive chromatin regulator of transcription, suppresses the expression of several genes involved in cell cycle regulation and the p53 pathway and (3) a new role for SETD1A in regulating tumour growth. This evidence concerns the gene TP53 and neoplasm.