It is also worth noting that in the context of RAS-overexpression and doxorubicin-induced senescence, the authors found that knockdown PTBP1 could reduce SASP and inhibit inflammation-driven cancer by promoting the exon inclusion of EXOC7, and no more cellular senescence phenotypes could be observed (such as cell growth arrest, higher SA-β-galactosidase activity, and upregulation of CDKN1A and CDKN2A) [38]. This evidence concerns the gene CDKN2A and cancer.