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These therapies reduce infection burden, especially from\n                    <jats:italic>Pseudomonas aeruginosa<\/jats:italic>\n                    , through enhanced mucociliary clearance and immune responses. Yet,\n                    <jats:italic>P. aeruginosa<\/jats:italic>\n                    often persists, raising concerns about microbial adaptation. Emerging evidence suggests that modulator-altered airways impose novel selective pressures, favouring mutations in genes linked to biofilm formation, iron metabolism and immune evasion. This may drive the emergence of strains adapted to a \u2018hybrid\u2019 airway; neither fully CF-like nor fully healthy. Such adaptations could potentially increase transmissibility or virulence, with implications beyond the CF population. Understanding how pathogens evolve under modulator pressure is essential in this new treatment era. 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