Angiogenesis-specific gene function was also implicated by the M2-like transcript abundance of GPRC5C, identified as a gene suppressed by estrogen receptor activation and capable of slowing MCF-7 growth (Yamaga et al., 2014), and a close paralog of GPRC5 family genes GPRC5A and GPRC5B, with more established roles in cancer to date (Acquafreda et al., 2009; De Francesco et al., 2017; Hirabayashi and Kim, 2020), including dysregulation of ceramide production in a GPRC5B-deficient model (Kim et al., 2018). The gene discussed is GPRC5A; the disease is cancer.