The association between Hashimoto's thyroiditis (HT) and papillary thyroid carcinoma (PTC) and whether HT can promote the occurrence and development of PTC have been a controversial topic for many years. In recent years, many studies have confirmed that there is a close relationship between HT and the occurrence and development of PTC. Tumorigenesis can be regarded as the joint outcome of the abnormal features of tumor cells, the influences of the formation of tumor microenvironment and external environmental factors. HT is considered as a chronic inflammatory reaction, and various inflammatory cells infiltrating around the thyroid gland of HT patients will damage the DNA of interstitial cells, leading to the wrong repair of DNA, thus promoting the occurrence of PTC. Tumor microenvironment plays a key role in different stages of tumorigenesis and development of tumors by affecting immune surveillance and tumor diffusion. Chemokines produced by PTC-associated macrophages and mast leukocytes can induce the production of various immune cells. The complex interaction between infiltrating immune cells and PTC cells has become an important factor affecting the occurrence and development of PTC. In terms of molecular mechanism, HT promoting the occurrence and development of PTC is related to RET gene rearrangement, p63 protein expression, RAS, BRAF gene mutation and PI3K/Akt expression. In the aspect of immune mechanism, CD3+, CD4+ and Th17 cells were found to play important roles in the occurrence and development of PTC. As for the endocrine aspect, the increase of thyroid-stimulating hormone (TSH) caused by long-term HT is also an independent risk factor for the occurrence, development, and postoperative recurrence of PTC. As regards to the big clinical data, HT is an independent risk factor for PTC, and the incidence rate of PTC was significantly higher in patients with HT. At the same time, the prevalence of HT in patients with PTC was significantly higher than that in patients without PTC. Paraffin pathology found that patients with PTC nodules and concomitant HT had better clinicopathologic features and prognosis than those with lone PTC nodules. The patients with PTC and HT had a higher incidence of multifocality of malignant nodules, but the patients with PTC and HT had a lower incidence of central lymph node metastasis, smaller nodule diameter and lower incidence of distant metastasis. The mutation rate of BRAFV600E gene was lower in PTC nodules of these patients, which indicate that HT have a good protective effect on the prognosis of PTC patients. The correlation between HT and PTC is a hot topic in thyroid research. In recent years, many scholars have conducted a lot of studies on the molecular mechanism. Relevant clinical features can further guide clinicians to judge the clinical characteristics and prognosis of PTC patients. Fully understanding the correlation between HT and PTC will help to deepen the understanding of the pathogenesis of PTC and provide new ideas and methods for immunotherapy of PTC.