My research focuses on autophagy (intracellular self-digestion), within which I primarily examine crinophagy, its regulation, and its relationship to the ubiquitin-proteasome system. Malfunction of autophagy appears as a causal factor in the pathomechanism of many diseases or contributes to the development of the disease and the exacerbation of symptoms. Excessive crinophagy, for example, plays a role in excessive insulin degradation within β-cells that cause type II diabetes and early activation of pancreatic enzymes, leading to the development of acute pancreatitis. Our main goal is to explore the regulatory pathways of crinophagy, thus bringing us closer to understanding the pathomechanism of these diseases and thus more effectively treating diseases that occur mainly in gland cells with defective crinophagy.