We focused on p53 as a target factor based on previous studies for the following reasons: (i) wild-type p53 transcriptionally regulates the EGFR gene via direct DNA binding [37–39]; (ii) p38 MAPK enhances p53 protein stability and transcriptional activity via the phosphorylation of N-terminal residues [40, 41]; (iii) co-overexpression of p53 protein and EGFR correlated with poor prognosis and advanced pathological stage in papillary thyroid carcinomas and NSCLC [42, 43]; and (iv) the p38 MAPK/p53/p21 signaling axis confers primary resistance to PTX in prostate cancer cells [44]. This evidence concerns the gene EGFR and differentiated thyroid carcinoma.