A study published in *Nature* (2010) reveals that non-coding RNAs, including those from pseudogenes, can regulate tumour biology by competing with microRNAs for binding, independent of their protein-coding function. The research focuses on the interaction between the mRNA of the PTEN tumour suppressor gene and its pseudogene, PTENP1. PTENP1 is biologically active, regulating PTEN levels and exerting a growth-suppressive effect. The PTENP1 locus is selectively lost in human cancers, suggesting its role in tumour suppression. The study extends this finding to other cancer-related genes, such as KRAS, showing that their pseudogenes also regulate gene expression. The 3'UTR of PTENP1 acts as a decoy for microRNAs that target PTEN, thereby increasing PTEN levels and suppressing tumour growth. This mechanism is conserved in other pseudogenes, such as those of OCT4 and KRAS, which also compete with their cognate genes for microRNA binding. The findings highlight the non-coding function of mRNAs and the potential of pseudogenes as regulators of gene expression in cancer. The study also demonstrates that pseudogenes can function as endogenous microRNA sponges, influencing the availability of microRNAs and their targets. These results suggest that pseudogenes may play a significant role in tumour suppression and that their expression and genomic status should be systematically studied in cancer research. The study provides a framework for understanding the broader role of endogenous mRNA in cellular biology, including the regulation of microRNA activity and the impact of pseudogenes on tumour progression.A study published in *Nature* (2010) reveals that non-coding RNAs, including those from pseudogenes, can regulate tumour biology by competing with microRNAs for binding, independent of their protein-coding function. The research focuses on the interaction between the mRNA of the PTEN tumour suppressor gene and its pseudogene, PTENP1. PTENP1 is biologically active, regulating PTEN levels and exerting a growth-suppressive effect. The PTENP1 locus is selectively lost in human cancers, suggesting its role in tumour suppression. The study extends this finding to other cancer-related genes, such as KRAS, showing that their pseudogenes also regulate gene expression. The 3'UTR of PTENP1 acts as a decoy for microRNAs that target PTEN, thereby increasing PTEN levels and suppressing tumour growth. This mechanism is conserved in other pseudogenes, such as those of OCT4 and KRAS, which also compete with their cognate genes for microRNA binding. The findings highlight the non-coding function of mRNAs and the potential of pseudogenes as regulators of gene expression in cancer. The study also demonstrates that pseudogenes can function as endogenous microRNA sponges, influencing the availability of microRNAs and their targets. These results suggest that pseudogenes may play a significant role in tumour suppression and that their expression and genomic status should be systematically studied in cancer research. The study provides a framework for understanding the broader role of endogenous mRNA in cellular biology, including the regulation of microRNA activity and the impact of pseudogenes on tumour progression.