Many additional mechanisms, however, have been found to contribute to the development of therapy resistance, including activation of the phosphoinositide 3-kinase (PI3K)‒AKT‒mammalian target of rapamycin (mTOR) pathway, tumor microenvironment reprogramming by the Hippo signaling pathway, and phenotype switching by master transcription factors (TFs), such as microphthalmia-associated transcription factor (MITF), and receptor tyrosine kinase (RTK), such as AXL [11]. The gene discussed is MTOR; the disease is neoplasm.