Furthermore, mating Tax transgenic mice with p53-deficient mice demonstrated minimal acceleration in initial tumor formation, but significantly accelerated disease progression and death in mice heterozygous for p53 suggesting that functional inactivation of p53 by HTLV-1 Tax, is not critical for initial tumor formation, but contributes to late-stage tumor progression (Portis et al., 2001). The gene discussed is CNTN2; the disease is neoplasm.