Evidence indicates that potentiated FGF2-FGFR1 signaling within the tumor cells contributes to the malignant phenotype through two specific molecular routes: it stimulates cellular proliferation through the AKT/MAPK cascade and enhances motility through the RAC1/CDC42 system (Jimenez-Pascual and Siebzehnrubl, 2019). The gene discussed is AKT1; the disease is neoplasm.