Although the present study clearly demonstrates that miR-196a-3p agomir inhibits and miR-196a-3p antagomir increases the expression of DHFR in adherent cells, future investigations are required to see whether GBM tumorspheres with DHFR re-expression from miR-196a-3p antagomir no longer rely on exogenous methionine. Here, DHFR is linked to glioblastoma.