CSs share the fundamental properties of SCs, but their activity contributes to the cancer grow and maintenance instead of replenishing normal cell pool.40 Moreover, teratomas generated from p53 knockout iPSs showed the presence of double-strand DNA breaks and DDR activation, leading to the conclusion that p53 inhibition decreases genomic stability.41 Due to the high risk of tumor generation after transplantation, methods utilizing p53 inhibition in iPSs generation seem to be unsuitable for therapeutic use. The gene discussed is TP53; the disease is neoplasm.