Cancer undergoes an evolutionary process during its progression. Initially they arise from foci of dysplasia in situ disease. Some of these indolent epithelial cells, will eventually “collect” additional aberrations over time. Among these cells, the ones with capability to adapt and are compatible within the local microenvironment will survive and proliferate, constantly adding novel altered biological properties, leading to more aggressive tumors. Scientists have long tried to identify driver events in cancer progression. Some driver mutations have been extensively studied, but a universal model has not emerged. One reason for this could be the huge heterogeneity among different clones in a single patient, as well as the fact every patient has unique tumor hallmarks. Apart from this, not all genetic aberrations cause phenotypic alterations, or confer survival advantage, but are neutral. Moreover, epigenetic and metabolic events have been found to independently affect the fate of tumor cells. Roughly the same principles apply in bacterial adaptation, speciation, evolution, etc. Various changes are observed but at the end of the end they all share something in common. If the newly introduced chemical reaction, chemical pathway, system etc, leads to increased survival of the whole system, then it will be selected, no matter what the cause of this change was. So we only have chemical changes that cause a favorable result and chemical changes that cause unfavorable results for the cell….So evolution can be reduced down to evolution and selection of the fittest chemical reaction systems.