Even when one considers angiogenesis and a whole series of paraneoplastic events that evolve via transformation in their own right, the actual generation of a neoplastic lesion would be best viewed perhaps as a series of cell fusion/hybridization events. In such terms, DNA events would recombine and induce aneuploidy not simply via systems of aberrant proliferative activity but rather via pathways of aberrant control or loss of control at cell cycle checkpoints. Indeed, in terms especially of qualitative alterations of a meiosis-type series of events coupled to quantitative increases in cell proliferative rates, one might better view neoplastic generation a specific form of progression that develops in a setting of a whole series of epigenetic phenomena ranging from angiogenesis to stromal desmoplasia to metastatic spread. Neoplasia would constitute a de-suppression of pathways of progression in terms of aberrant cell cycle entry at checkpoints and also of aberrant cell cycle progression involving specifically cell fusion/hybridization events.