Additionally, we found that FDY003 may target key signaling cascades connected to the diverse LC pathological mechanisms, namely, phosphoinositide 3-kinase (PI3K)-Akt, focal adhesion, interleukin (IL)-17, forkhead box O (FoxO), mitogen-activated protein kinase (MAPK), and tumor necrosis factor (TNF) pathways. The gene discussed is AKT1; the disease is laryngotracheoesophageal cleft.