In fact, GATA6-AS1 (and GATA6) expression was shown to be controlled by two distinct mechanisms: lower expression in basal-like tumours might be caused by higher DNA methylation near the GATA6 gene, whereas classical tumours showed copy number gains of the GATA6 neighbourhood in conjunction with higher expression of GATA6 mRNA as well as GATA6-AS1 in the classical subtype [3]. Here, GATA6 is linked to neoplasm.