Mechanistic analysis revealed that METTL3‐mediated m6A modification of PCAT6 led to the upregulation of PCAT6 in an IGF2BP2‐dependent manner and PCAT6 enhanced the stability of IGF1R mRNA by interacting with IGF2BP2. Clinically, the correlation of the m6A/PCAT6/IGF1R axis with PCa was further verified in PCa tissues and cells. The gene discussed is IGF1R; the disease is posterior cortical atrophy.