Vibrio cholerae is the causative agent of cholera and thrives in both aquatic environments and the human intestinal tract. The most prominent predatory phage found in cholera patient stool samples with V. cholerae is ICP1. In order to combat ICP1 predation, V. cholerae has evolved a unique defense system referred to as the PLE (Phage-inducible chromosomal island Like Element). PLE is an ~18-kb genomic island that is found integrated into the small chromosome of clinical isolates of V. cholerae. Five PLE variants have been identified and are characterized by the ability to respond specifically to ICP1 infection and inhibit progeny phage production. We hypothesize that PLE encoded regulators keep the island quiescent during normal cellular growth in the absence of phage, and, upon infection, phage proteins interact with the regulators to alleviate repression ultimately leading to the induction of PLE activity. We found that ICP1 isolates display unique susceptibility patterns to different PLEs, indicating that ICP1 isolates may have evolved to evade PLE induction. To identify PLE induction cues, we exploited the differences in host range between phage isolates to generate recombinant phage with altered induction phenotypes. We constructed a randomly sheared genomic library of non-inducing phage and introduced it into PLE- V. cholerae. Inducing phage were propagated in the presence of the genomic library, allowing for recombination between isolates. The resulting lysate was screened on PLE+ V. cholerae to identify recombinant phage that fail to induce the PLE. Using this method, we isolated recombinant phages that are no longer blocked by PLE2. We investigated the ability of these recombinants to induce other PLEs and propose whole-genome sequencing to identify recombinant regions and determine the induction cue.