Activation of EGFR could induce SALL4 overexpression by the extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway, while SALL4 knockdown could not only inhibit spheroid formation and the expression of CD44, a type of lung cancer stem cell marker, but also increase the sensitivity of EGFR-mutated cells to EGFR inhibitor erlotinib [15]. This evidence concerns the gene SALL4 and lung cancer.