Prevalent mechanisms of oncogenic TK activation (i.e., gene amplification, chromosomal rearrangements, gain of function mutations, and autocrine activation or aberrant ligand production in the tumor microenvironment) suppress immune surveillance and enhance tumor cell survival, proliferation, motility and invasion in a wide spectrum of cancers and thereby drive tumor progression, metastasis and drug resistance [46–48]. The gene discussed is TKT; the disease is neoplasm.