CFTR and cystic fibrosis: Malfunctioning of the CFTR, along with accumulation of the misfolded channel, in the case of ΔF508 homozygous patients, induces a perpetual chronic low-grade inflammation in CF macrophages, predisposing these cells to a hyper-inflammatory and metabolic response, driven by XBP1s, which is exacerbated by the activation of TLR4 (Figure 7) and may be unresolved due to the lack of M2 macrophage polarization.