Here we described a novel molecular mechanism driving the ontogeny of AXL-positive EGFR TKi-resistant cells based on the stochastic fluctuation of cancer cells between an AXL-negative state characterized by epithelial-like features and an AXL-positive state in which cells are mesenchymal and have an increased resistance to EGFR TKi (Figure 7). The gene discussed is AXL; the disease is cancer.