However, none of the conditioned media altered CD8+ T-cell proliferation (Supplementary Fig. 12c, d), arguing against a direct, soluble factor-mediated, VHL- or HIF-α-dependent cross-talk between ccRCC and T cells as being the mechanism that underlies the altered immune microenvironment in the Vhl∆/∆Trp53∆/∆Rb1∆/∆Hif1a∆/∆ and Vhl∆/∆Trp53∆/∆Rb1∆/∆Hif2a∆/∆ tumours. The gene discussed is VHL; the disease is neoplasm.