Mechanistic investigations have revealed that the oncogenic proliferation of lung cancer cells induced by FAM83A upregulation is primarily attributed to the aberrant activation of several growth-related signaling pathways, including Hippo, Wnt, Extracellular regulated protein kinase (ERK), and PI3K/Protein kinase B (AKT)/Mammalian target of rapamycin (mTOR) signaling pathways [39–41]. The gene discussed is SACK1A; the disease is lung cancer.