The phosphatase-deficien mutant, ΔE6, was also observed with high frequency in both colon and thyroid tumors, unexpectedly, although the ΔE6 mutant was incapable of dephosphorylating p-Tyr527 of Src (Fig 5), ΔE6 overexpressing cell lines were tumorigenic and formed tumors that rapidly grew at the same rate as those induced by PTP1B WT and PTPα, which can activate Src directly as we have previously reported [9,18]. This evidence concerns the gene SRC and thyroid tumor.