The Pim‐1 proto‐oncogene is one of the most potent collaborators of the myc proto‐oncogenes in inducing lymphomagenesis in mice. Contrary to the profound effects when overexpressed in vivo, Pim‐1‐deficient mice showed only subtle phenotypic alterations, which could indicate the presence of redundantly acting genes. In line with this, a PCR‐based screen has led to the identification of a closely homologous gene, Pim‐2. The X‐linked Pim‐2 gene is 53% identical to Pim‐1 at the amino acid level and shares substrate preference and the usage of non‐AUG initiation codons with Pim‐1. We have used these data to test whether the strong synergistic interaction between Pim‐1 and c‐myc can be utilized to gain access to Pim‐1 compensatory pathways. We reasoned that, upon proviral tagging in compound mutant mice (E mu‐myc/Pim‐1‐/‐ mice), the selective advantage of cells carrying provirally activated genes, that act downstream from or parallel to Pim‐1, would increase. We show here that this is the case. A dramatic increase (from 15 to 80%) was found in the frequency of proviral activation of the Pim‐2 gene. These data show that the described strategy of ‘complementation tagging’ represents a powerful new tool to identify components of pathways involved in processes as complex as multistep tumorigenesis.