Two recent studies of SPI1(PU.1) regulation in AML revealed functional roles for a noncoding RNA transcribed from an antisense promoter (asRNA) in the third exon of the gene and a lncRNA termed LOUP that is transcribed from a promoter/enhancer element 17 kb upstream from the SPI1 promoter [35,36]. The gene discussed is SPI1; the disease is acute myeloid leukemia.