HOTAIRM1 and central nervous system cancer: The in vitro data are in line with studies reporting on tumor-promoting functions of TGM2 in other cancer models [48, 49] and suggest regulation of TGM2 by HOTAIRM1 as a putative mechanism driving glioma aggressiveness However, TGM2 expression is not regulated by promoter methylation in patient samples, as analysis of glioblastoma methylation data showed that HOTAIRM1 promoter is unmethylated in all samples, independently of high or low HOTAIRM1 expression (Supplementary Fig. 7C).