For instance, the N546K mutation accelerates the formation of monophosphorylated FGFR1 receptors 25-fold faster than the wild-type, leading to constitutive activation of FGFR1, while the K656E [9,18] mutation enhances autophosphorylation levels, resulting in constitutive activation of FGFR1 These mutations are observed across multiple diseases, notably in Encephalocraniocutaneous lipomatosis (ECCL), including conditions like scalp lesions, benign eye tumors, and central nervous system lipomas. This evidence concerns the gene FGFR1 and benign neoplasm of eye.