Data about G-CSF involvement in ROP is controversial: G-CSF vitreous levels were increased in ROP patients and are associated with ROP-related inflammation [47, 48], and G-CSF deficiency had a partial protective effect in animal model of ROP [49], but at the same time G-CSF can be given to premature infants as a clinical treatment, and in such infants there was a trend (though insignificant) for reduced need in laser treatment for ROP [50]. The gene discussed is CSF3; the disease is retinopathy of prematurity.