We speculate that although senescence serves as a powerful tumor suppressor, it also confers certain survival advantages on cancer cells that have not yet completed stem transformation, such as through the activation of target involved in stemness-related programs, such as MYC, STAT3, WNT, and NOTCH, allowing them to evade excessive DNA damage during the maintenance of the senescent state, have stronger proliferative abilities after the necessary maintenance conditions are eliminated, and subsequently to refill the human body. This evidence concerns the gene MYC and neoplasm.