Sandra Molle

Correction to: Nature https://doi.org/10.1038/s41586-025-08931-1 Published online 7 May 2025 Following publication of this article, the Protein Data Bank entry originally listed in the article (9BTP, in Fig. 4 caption, Methods, Data Availability, Extended Data Table 2 and Reporting Summary) was updated to a new entry: 9OVJ. Accession codes have been updated throughout the paper and data in Extended Data Table 2, the 9OJV column, have been updated in the HTML and PDF versions of the article.

Abstract Activating mutations in the rat sarcoma (RAS) genes HRAS, NRAS and KRAS collectively represent the most frequent oncogenic driver in human cancer1. They have previously been considered undruggable, but advances in the past few years have led to the clinical development of agents that target KRAS(G12C) and KRAS(G12D) mutants, yielding promises of therapeutic responses at tolerated doses2.