Similarly, Burkholderia cepacia (B. cepacia), an opportunistic infection that afflicts 3–5% of CF patients, can provoke exacerbations [151]. It has been found that macrophages can kill B. cepacia within autophagolysosomes; however, macrophages with ΔF508-CFTR lacked the bacteria in autophagolysosomes indicating dysfunction [151]. When these macrophages were treated with the autophagy inducer rapamycin, ΔF508-CFTR macrophages were able to fight the B. cepacia infection and reduce the resulting inflammation [153,179]. This demonstrates the importance of CFTR-dependent autophagy in not only clearing bacteria that can provoke pulmonary exacerbations, but also decreasing inflammation that can lead to worsened lung functions as well.