Figure 1 displays the mechanisms of p53 in response to DNA damage in SCLC cells. These are occasionally accompanied by a 3p deletion (Whang-Peng et al., 1982) and when they are deleted, the mechanism indicated in Figure 1 is not able to inhibit cell growth or uncontrolled cell proliferation, and consequently there is tumor growth and disease progression. P53 and RB1 deficient SCLC tumors may also express increased cKit (Rao et al., 2020), MYC amplification (20% of patients (Pietanza et al., 2015)), and loss of phosphatase and tensin homolog (PTEN). This evidence concerns the gene PTEN and neoplasm.