TGFBR3 and neoplasm: ADAMTS9-AS2 was previously found dysregulated in several cancer types including NSCLC.32,33 Overexpression of ADAMTS9-AS2 reduces proliferation, cell migration, invasion, and induces apoptosis in vitro while restrains tumour growth in vivo.32–34 Recent evidence suggests that ADAMTS9-AS2 might exert its function by ‘sponging’ common microRNAs.33,34 For instance, in NSCLC, ADAMTS9-AS2 represses cancer progression by regulating the miR-223-3p/TGFBR3 axis,33 while in ovarian cancer it regulates the miR-182-5p/FOXF2 pathway.34