GPC is also involved in another pathway: ether lipid metabolism (KEGG: hsa00565), where GPC can also be produced by conversion of 1-(1-alkenyl)-sn-glycero-3-phosphocholine by TMEM86B. However, this gene does not show a significant change between PCa tissue and normal tissue, and hence we can explain the elevated levels of GPC by the extracted part of glycerophospholipid metabolism shown in the case study. The gene discussed is TMEM86B; the disease is posterior cortical atrophy.