While it is acknowledged that this scenario is highly speculative and would require in-vivo confirmation as well as further characterization of the SAOS-2 response to TNF-α, current data together with our separate report of altered cytokine synthesis by h-GF permitted cellular sipping [14], do highlight the extreme complexity of interactions between neoplastic and stromal cells and suggest at least partial explanation for the great morphological variability seen within different domains of single neoplasms in-vivo [38]–[40]. The gene discussed is TNF; the disease is neoplasm.