Siraj M Ali

Correction to: Nature https://doi.org/10.1038/s41586-022-05066-5 Published online 10 August 2022 This paper was originally published under a standard Springer Nature license (© The Author(s), under exclusive licence to Springer Nature Limited). It is now available as an open-access paper under a Creative Commons Attribution 4.0 International license, © The Author(s). The error has been corrected in the HTML and PDF versions of the article.

Abstract Somatic hotspot mutations and structural amplifications and fusions that affect fibroblast growth factor receptor 2 (encoded by FGFR2) occur in multiple types of cancer1. However, clinical responses to FGFR inhibitors have remained variable1,2,3,4,5,6,7,8,9, emphasizing the need to better understand which FGFR2 alterations are oncogenic and therapeutically targetable.

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