Asthma is a chronic obstructive airways disease characterized by symptoms: shortness of breath ("whistling"), loss of breath, coughing, chest tightness and sputum production. Asthma is a global disease that affects people unevenly regardless of race, age, gender, ethnicity, or geographic location. It is estimated that between 2-18% of the world's population suffers from asthma. The ISAAC program is the first global study of asthma prevalence whose worrying data led to a major focus on asthma in the early 21st century. The etiology of asthma depends on two main factors: genetics and the environment. Their intertwining gives a broad external and internal phenotyping of the disease as well as a complicated classification of the severity of asthma. There are a number of GINA patterns for diagnosing a particular type of asthma as well as the prescribed dosage therapy for it. Today’s diagnosis of asthma is based on functional lung tests and a wide range of bronchoprovocation tests with the assistance of modern tools such as biomarkers and OMIC methods in identifying the specific pathophysiological mechanism of inflammation. The most common external causes of asthma are: allergens, pollutants and microorganisms (especially viruses and bacteria). Allergic asthma is the most common type of asthma with the highest growth trend in patients (especially children). Asthma genetics have been studied in: association studies, association studies (GWAS), and epigenetic studies. Asthmatic inflammation is divided into Th1 and Th2 type responses. While the Th1 response is not so well known, the Th2 response has been studied from the etiological and therapeutic side. Many immune cells participate in the Th2 response, and the most influential are: T-lymphocytes, eosinophils and mast cells. Smooth muscle, epithelial, and subepithelial cells of the airways are the most affected tissues in asthmatic inflammation, mediated by proinflammatory cytokines, causing airway closure and limited airflow. The JAK / STAT signaling pathway is crucial for asthmatic inflammation. The receptor-ligand initiation signal initiates receptor multimerization, consequetnly activating a cascade pathway of JAK kinase phosphorylation that causes activation of the STAT transcription key in the transcriptional expression of cytokine-inducing genes. Disruption of this signal in asthma leads to strong migration of immune cells and production of cytokines in the bronchi. Jak-inhibitors in asthma aim to prevent the very initiation of JAK / STAT inflammation, unlike previous symptomatic therapies. Currently known strong inhibitors in clinical, preclinical or patent applications are: Theravance: TD-8236, Rigel / AstraZeneca: R256 / AZD0449, AstraZeneca: "Example 35", Almirall: LAS194046, Vectura: VR588, Merck: iJAK-001 and IJC- 1, Genentech: iJAK-381 and GDC-0214 and PM-43I as the sole STAT inhibitor.