In cancer cells, aberrant activation of FGF/FGFR signaling caused by FGFR amplification, activating FGFR mutations, FGFR single-nucleotide polymorphisms, FGFR fusion protein formation with various binding partners, and deregulation of phospholipase Cγ1 (PLCγ1, FRS1) and FGFR substrate 2 (FRS2) all promote cell survival, cell proliferation, angiogenesis, acquisition of an epithelial-mesenchymal transition (EMT) phenotype, invasion, and metastasis in cancer cells124,126. This evidence concerns the gene PLCG1 and cancer.