In fact an autoregulatory mechanism between these two proteins has been identified, in this process VRK1 can not induce a permanent block of cell cycle progression by accumulation of a stabilized p53, because p53 induces proteolytic degradation of VRK1 [20], a mechanism that is disrupted in lung carcinomas with TP53 mutations [21]; therefore in tumors with mutations in p53 there is an accumulation of a protein, VRK1, necessary for cell division, and thus might contribute to tumor cell expansion. Here, TP53 is linked to neoplasm.