Tyrosine kinases (TKs) are enzymes that catalyze the transfer of phosphate from ATP to tyrosine residues in proteins. They play critical roles in cellular processes such as proliferation, survival, and differentiation. Over 25 years ago, TKs were implicated in oncogenesis in animal tumors caused by retroviruses, but they were not widely considered as therapeutic targets due to limited evidence of their role in human cancer and concerns about drug specificity and toxicity. This changed with the success of imatinib mesylate, which targets the BCR-ABL TK in chronic myeloid leukemia (CML), marking a breakthrough in targeted cancer therapy. TKs are now recognized as important targets for cancer therapy. They are divided into receptor and nonreceptor types, with receptor TKs being transmembrane proteins and nonreceptor TKs found in the cytosol and plasma membrane. TK activity is tightly regulated, and dysregulation can lead to cancer. Common mechanisms of TK dysregulation include chromosomal translocations, mutations, and overexpression. For example, in CML, the BCR-ABL fusion TK is constitutively active due to a chromosomal translocation. In AML, mutations in FLT3 can lead to constitutive activation of the TK. Several strategies are used to target TKs in cancer therapy, including small-molecule inhibitors, monoclonal antibodies, and inhibitors of chaperone proteins like Hsp90. Imatinib, a small-molecule inhibitor, has shown significant efficacy in CML and other cancers involving BCR-ABL or c-KIT. However, resistance to TK inhibitors can develop due to mutations or other mechanisms, necessitating the development of second-generation inhibitors and combination therapies. TKs are also important targets in solid tumors, such as gastrointestinal stromal tumors (GISTs), where mutations in c-KIT or PDGFRα are common. EGFR inhibitors like gefitinib and erlotinib have shown efficacy in non-small-cell lung cancer, particularly in patients with EGFR mutations. Monoclonal antibodies targeting receptor TKs, such as trastuzumab for HER-2, have also been developed. Despite the promise of TK-targeted therapies, challenges remain, including toxicity, resistance, and the need for more effective and affordable treatments. The development of these therapies requires careful consideration of patient selection, pharmacodynamic monitoring, and the potential for combination therapies with other treatments. Future research aims to identify new TK targets, improve therapeutic strategies, and address the challenges of drug development and cost.Tyrosine kinases (TKs) are enzymes that catalyze the transfer of phosphate from ATP to tyrosine residues in proteins. They play critical roles in cellular processes such as proliferation, survival, and differentiation. Over 25 years ago, TKs were implicated in oncogenesis in animal tumors caused by retroviruses, but they were not widely considered as therapeutic targets due to limited evidence of their role in human cancer and concerns about drug specificity and toxicity. This changed with the success of imatinib mesylate, which targets the BCR-ABL TK in chronic myeloid leukemia (CML), marking a breakthrough in targeted cancer therapy. TKs are now recognized as important targets for cancer therapy. They are divided into receptor and nonreceptor types, with receptor TKs being transmembrane proteins and nonreceptor TKs found in the cytosol and plasma membrane. TK activity is tightly regulated, and dysregulation can lead to cancer. Common mechanisms of TK dysregulation include chromosomal translocations, mutations, and overexpression. For example, in CML, the BCR-ABL fusion TK is constitutively active due to a chromosomal translocation. In AML, mutations in FLT3 can lead to constitutive activation of the TK. Several strategies are used to target TKs in cancer therapy, including small-molecule inhibitors, monoclonal antibodies, and inhibitors of chaperone proteins like Hsp90. Imatinib, a small-molecule inhibitor, has shown significant efficacy in CML and other cancers involving BCR-ABL or c-KIT. However, resistance to TK inhibitors can develop due to mutations or other mechanisms, necessitating the development of second-generation inhibitors and combination therapies. TKs are also important targets in solid tumors, such as gastrointestinal stromal tumors (GISTs), where mutations in c-KIT or PDGFRα are common. EGFR inhibitors like gefitinib and erlotinib have shown efficacy in non-small-cell lung cancer, particularly in patients with EGFR mutations. Monoclonal antibodies targeting receptor TKs, such as trastuzumab for HER-2, have also been developed. Despite the promise of TK-targeted therapies, challenges remain, including toxicity, resistance, and the need for more effective and affordable treatments. The development of these therapies requires careful consideration of patient selection, pharmacodynamic monitoring, and the potential for combination therapies with other treatments. Future research aims to identify new TK targets, improve therapeutic strategies, and address the challenges of drug development and cost.