Recently, we developed a novel therapeutic strategy that targets KRAS and TP53 mutations at same time via liposome delivery of clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9), ribonucleoprotein (RNP) complexes, and single-guide RNA (sgRNA) to overcome drug-resistance of PDAC, and this treatment significantly enhanced the anti-tumor activity of gemcitabine [15]. This evidence concerns the gene KRAS and neoplasm.