The PSMA PET-CT negative lesions (27.5%) were postulated to be secondary to loss of PSMA due to neuroendocrine transdifferentiation (confirmed histologically in a single case where the metastatic deposit was biopsied [70]), however Pryka et al., (2016) demonstrated that due to high PSMA uptake in lung cancer, PSMA PET-CT was unable to differentiate between a lung primary lesion and PCa metastasis [71]. This evidence concerns the gene FOLH1 and posterior cortical atrophy.