RNA editing destroys the binding sites of miR‐25‐3p and miR‐125a‐3p in the 3’‐untranslated region (3’‐UTR) of DHFR, resulting in elevated DHFR levels.[21] In some cases, A‐to‐I editing could cause aberrant splicing of targeted mRNA resulting in drug resistance.[22] Collectively, A‐to‐I RNA editing has the potential to become a new nucleic acid‐based therapeutic target to reverse drug resistance in cancer. The gene discussed is DHFR; the disease is cancer.