MSH2 and neoplasm: Nonetheless the results of in vitro EV transfer experiments suggest that the TKI-resistant subclones could release EV with low miR-21-5p and high miR-486-3p, and a high level of lncRNAs MEG3 and XIST. The EV-RNAs then modulated TKI-sensitivity by inhibition of tumour suppressors PTEN and MSH2 of the recipient subclones and enhanced their survival.