To address this important deficiency, we first asked whether NanogP8 protein could be recognized by the 7 anti-Nanog1 Abs (except the BioLegend Ab) by taking advantage of our recent K14-NanogP8 transgenic (Tg) animal model in which the NanogP8 cDNA derived from a primary PCa (i.e., HPCa5) was driven by a cytokeratin 14 promoter [64]. The gene discussed is KRT14; the disease is posterior cortical atrophy.