Reduced Bcl-2 protein expression, appearance of cleaved caspase-3, upregulation of p53, and enhancing Bax, observed after WT1 silencing, are consistent with an oncogenic role of WT1, similarly to other investigated cell type [74–76], and in opposition to others, where WT1 could suppress Bcl-2 family protein functioning as a tumor suppressor [77]. The gene discussed is TP53; the disease is neoplasm.