These mutations promote tumorigenesis through multiple mechanisms: sustained MAPK-ERK pathway activation phosphorylates and activates transcription factors ELK1 and AP-1, upregulating proliferation-related genes; meanwhile, aberrant PI3K-AKT pathway activation inhibits apoptosis by phosphorylating BAD and FoxO3a, enhancing tumor cell survival [108,109]. The gene discussed is BAD; the disease is neoplasm.