Summary:

In this issue, Hattori and colleagues capitalized on targeted small-molecule covalent inhibitors of one KRAS mutant with a G12C substitution and of other oncoproteins to create drug–peptide conjugates that serve as cancer neoantigens that prompt an immune response to oncogene-mutant cancer cells. This immunotherapy strategy can serve as an effective approach to overcome the treatment-induced resistance that limits the effectiveness of essentially all small molecule–based targeted anticancer drugs.

See related article by Hattori et al., p. 132 (9).