RNA-binding proteins and post-transcriptional modifications also contribute to GAS5 regulation, with experimental systems employing CRC cell lines and murine models demonstrating that the m6A reader protein YTH-domain family member 3 (YTHDF3) negatively regulates GAS5 by inducing its decay [44], and studies using Lewis lung cancer Luciferase (LLC-Luc) cells and mouse models revealing that the Up-frameshift protein 1 (UPF1)-mediated NMD pathway participates in its modulation [41]. Here, GAS5 is linked to medical procedure.