Having documented selective effects of ERG on AR transactivation on AR half-site reporters, we next turned to a more physiologically relevant model of prostate cancer in which ERG overexpression drives a basal to luminal transition and transcription of a class of AR co-dependent genes whose ARE and ETS binding sites are separated by half a helical turn of DNA in primary mouse prostate organoids lacking Pten (Chen et al., 2013; Karthaus et al., 2014; Li et al., 2020; Mao et al., 2019; Wasmuth et al., 2020). The gene discussed is ERG; the disease is Familial prostate cancer.