Mechanistically, we found that TRAF3IP2-AS1 directly interacted with poly ADP-ribose polymerase (PARP1) mRNA, a known oncogene, to promote the mRNA decay by stimulating m6A modification, but, in NONO-TFE3 tRCC, low expression of TRAF3IP2-AS1 caused upregulation of PARP1 by decreasing the PARP1 mRNA decay. This evidence concerns the gene PARP1 and renal cell carcinoma associated with Xp11.2 translocations/TFE3 gene fusions.