In contrast, mutant RTKs, such as FLT3-ITD and c-KIT V617F found in AML and amplified MET found in gastric, lung, and hepatocellular carcinoma, are reported to evade lysosomal degradation by intracellular transport to endoplasmic reticulum (ER) or Golgi apparatus, and instead continue to propagate oncogenic signaling from these organelles [28,29,30,31,32]. The gene discussed is KIT; the disease is acute myeloid leukemia.