Some recent studies, indeed, have suggested that in respiratory virus-induced sepsis and pneumonia, the molecule interacts with several mediators including the epidermal growth factor (EGF), c-jun proto-oncogene, C-C chemokine receptor type 5 (CCR5), angiotensin II receptor type-2 (AGTR-2), and signal transducer and transcription activator 3 (STAT3) [201,211,212]. This evidence concerns the gene CCR5 and susceptibility to pneumonia measurement.