This process includes the interaction of genomic, environmental, and host factors that lead to mutations in BRAF, MYC, NRAS, ERBB4, PTPs, NF1, KIT, etc. The second step involves additional mutations that overcome tumor suppressor mechanisms, mainly through disruption of the p16 or RB1 pathway (CDKN2A, CDK4, CCND1, APC, etc.), allowing the cells to escape primary senescence and leading to a lifespan extension. The gene discussed is KIT; the disease is neoplasm.