For instance, gain‐of‐function mutations and overexpression of RAS family members (KRAS, HRAS, and NRAS) are among the most prevalent oncogenic lesions in human cancers (Prior et al., 2012), and high levels of Ras activity are necessary to maintain the transformed phenotype in some Ras‐driven cancers (Singh et al., 2009). Here, HRAS is linked to cancer.