Cell competition is a homeostatic mechanism, which non-autonomously determines the fate of the cells- to die (lose) or to thrive (win). This phenomenon was originally described 40 years ago to occur between wild type cells (winners) and cells that are haploinsufficient for ribosomal proteins (which are called Minute cells-losers). Since then, cellular differences in a handful of genes have been described to trigger cell competition. Previous members in our lab conducted an EMS unbiased genetic screen to identify mutations that permit the survival of Minute cells during cell competition. Interestingly, one of these mutations was mapped in the ribosomal protein gene RpS12. RpS12 homozygous mutant flies are viable, fertile, with no obviously identifiable phenotype. We are currently in the process of investigating the role of RpS12 in cell competition. By sucrose density gradient analysis, we have shown that the mutant form of RpS12 is able to assemble into the ribosomes in vitro (S2 cells) and in vivo (fly tissues). Our polysome analysis also showed that RpS12 exists in extra-ribosomal fractions. Our efforts are now being directed towards the characterization of the potential extra-ribosomal role of RpS12 by purification of RpS12 complexes. It is tempting to think RpS12 as an internal ribosome-quality control factor that helps to identify the less ribosome-efficient cells in the tissue and eliminate/restrict them for the flourishing of the organism.