Conversely, the two Wilms tumors showed two clearly distinct (coexisting) tumor cell populations with a common CD56+ and CD58+, CD45−, CD99−, GD2−, nuMYOD1−, numyogenin−, CD10− and NG2− phenotype, but distinct reactivity (negative versus positive expression) for CD90, EpCAM and CD57 (Table 2; Figures 1 and 2). This evidence concerns the gene EPCAM and neoplasm.