A recent study published in Cell on papillary thyroid cancers (PTCs) suggests that there are new markers of aggressive tumors that could lead to more targeted therapies for cancer patients. TCGA researchers identified the presence of several new oncogenes and their variants based on the analysis of PTCs, and that they could also explain 80% of all types of thyroid cancer. These new findings suggest that thyroid cancers can be reclassified at the molecular level to better reveal tumor markers and their respective characteristics. This also gives us new perspectives on how observing how proto-oncogenes change and thus contribute to disease progression can lead to a better understanding of the biological causes of cancer, and by exploring the genetic and cellular similarities and differences in each type of tumor, can give researchers more information on how to individualize treatment for cancer patients. Thyroid incidence on the rise The incidence of thyroid cancer has nearly tripled over the past three decades, and in the United States there are nearly 20,000 new cases of PTC each year, a disease that can be treated with surgery, thyroid hormones and radiation with a five-year survival rate of more than 95 percent. Previous studies have shown a high frequency of genetically encoded effects that induce changes in the body, including point mutations in BRAF and RA5 genes, and complex kinase RET and NJRKI fusions. alterations in the MAPK pathway are closely associated with clinicopathological features, gene expression, and DNA methylation. Other studies have similar analyses, such as altered gene copy number, mRNA, miRNA and protein expression and DNA methylation. The genetic cause of PTC is known Studies have shown that PTC is mainly caused by BRAF or RA5 mutations. Some investigators have largely confirmed all mutations in papillary thyroid cancer, which is significant for diagnosis at the molecular level and beyond. BRAF and RA5 are mutually exclusive in PTC but share signaling pathways, for which investigators explore which gene the tumor prefers by looking for gene expression signals. Mutations may be the biological basis for the clinical manifestations of PTC patients, and many people are working on molecular diagnostics, we will have a broader genetic prospect, and molecular testing will provide us with more information. PTC is not a “uniform, homogeneous” cancer Based on this powerful finding, a pathological reclassification of follicular thyroid lesions is warranted. Refining the classification scheme to more accurately reflect differences between genotype and phenotype will help to implement more precise surgical and pharmacological treatments for PTC. Our study has shown that there are at least four molecular subtypes of PTC, so it can no longer be assumed that PTC is a uniform, homogeneous cancer.