Among these, LINC‐PINT (amplified in 3.3% samples of GBM), TRAF3IP2‐AS1 (deleted in 2.8% samples of LUAD) and TP53TG1 (amplified in 4.0% samples of LUSC), which have been recorded in known cancer lncRNA databases, were nominated for mutual exclusivity with established cancer PCGs, such as EGFR for LINC‐PINT, PIP5K1A for TRAF3IP2‐AS1 and BCL2 for TP53TG1, suggesting that these infrequent candidate driver lncRNAs harbored functionally redundant genetic lesions with known cancer PCGs and conferred similar selective growth advantage for tumor cells. This evidence concerns the gene BCL2 and cancer.