Colorectal cancer (CRC) is one of the most common cancers with high morbidity and mortality rates. The rates of early diagnosis of the disease have increased considerably after technological developments and studies. However, a significant portion of the cases is still diagnosed at an advanced stage. Therefore, studies have focused especially on the molecular pathogenesis of the disease. Colorectal cancers are a heterogeneous and multifactorial disease group. CRCs can occur in different forms, familial or sporadic. Three different molecular pathways have been identified, namely the Chromosomal Instability (CIN) pathway, the Microsatellite Instability (MSI) pathway, and the CpG Island Methylator Phenotype (CIMP) pathway, which play a role in the development of CRC. There is a mechanism by which many genes are effective in the etiopathogenesis of the disease. Among the genes associated with the disease, especially APC, KRAS, NRAS, BRAF, TP53, and DNA mismatch repairs genes such as MLH1, MSH2, MSH6, and PMS2 are involved in these molecular pathways. Understanding the molecular basis of colorectal carcinogenesis is important for the diagnosis, prognosis and treatment of the disease. Therefore, these genes have taken their place in the disease guidelines used in the clinic today. The molecular methods by which genetic changes in these genes can be detected and the algorithms to be followed according to the result are explained in detail in the guidelines. However, promising studies continue to elucidate the molecular mechanisms of colorectal cancers and personalized targeted therapy methods.