In the context of neoplasms, evidence indicates that PPAT–prostate inter-organ communication plays a significant role in driving prostate cancer (PCa) development and progression [1,3], which is further amplified in obesity, as “obese” PPAT presents heightened secretion of pro-inflammatory and tumorigenic factors [1,4], nurturing a pro-tumorigenic niche. The gene discussed is PPAT; the disease is posterior cortical atrophy.