Functional studies have suggested that tumor cells with these mutations are less responsive to estrogen deprivation as induced by aromatase inhibitors (AIs) (Robinson et al., 2013; Toy et al., 2013), but may still experience growth inhibition by ER‐blocking agents such as tamoxifen and fulvestrant (Jeselsohn et al., 2014; Robinson et al., 2013; Toy et al., 2013). Here, ESR1 is linked to neoplasm.