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. 2021 Apr 2;128(7):1040–1061. doi: 10.1161/CIRCRESAHA.121.318051

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© 2021 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 3. — Hypothesized mechanisms underlying the prohypertensive effects of various classes of antineoplastic drugs and adjuvant therapies (Illustration credit: Ben Smith). BRAF indicates v-raf murine sarcoma viral oncogene homolog B1; BTK, Bruton's tyrosine kinase; MEK, mitogen-activated protein kinase kinase; mTOR, mammalian target of rapamycin; PARP, poly ADP ribose polymerase; RET, rearranged during transfection; and VEGF, vascular endothelial growth factor.