Casp1, also known as Caspase-1, is a gene encoding proteins related to cell death. It plays a key role in caspase-1 mediated classical pyroptosis, an important programmed cell death process. Casp1 is associated with various pathways, such as those related to inflammation, immune response, and apoptosis [2,5]. It is involved in the activation of the NLRP3 inflammasome, which is fundamental for interleukin-1β maturation and subsequent inflammatory events [4].

In pancreatic cancer, knockdown of Casp1 inhibited cell viability and migration, and enhanced gemcitabine-induced cell death. Activating Casp1 with a DPP8/DPP9 inhibitor also increased gemcitabine-induced cell death by pyroptosis, suggesting it could be a target for combination therapy [1]. In acute promyelocytic leukemia, ATRA treatment increased and activated Casp1, triggering pyroptosis and differentiation of APL cells, indicating it may act as a suppressor in APL progression [2]. In acute myeloid leukemia, high CASP1 expression was associated with poor prognosis and its inhibition impaired cell proliferation [5]. In atherosclerosis, CASP1 was highly expressed, and the higher its expression, the worse the prognosis [3].

In conclusion, Casp1 is crucial in programmed cell death, especially pyroptosis, and inflammation-related pathways. Gene-knockout studies in various disease models, like pancreatic cancer, leukemia, and atherosclerosis, have revealed its role in disease development, prognosis, and potential as a therapeutic target. These findings contribute to a better understanding of disease mechanisms and the exploration of new treatment strategies.