Casp1, also known as Caspase-1, is a gene encoding proteins related to cell death. It is involved in pyroptosis, a type of programmed death, and is a key component of the NLRP3 inflammasome which is important for interleukin-1β maturation and inflammatory events. It participates in regulating various biological processes such as the innate immune response [5].

In pancreatic cancer, knockdown of Casp1 inhibits cell viability and migration, and enhances gemcitabine-induced cell death, suggesting its potential as a target for combination therapy [1]. In acute promyelocytic leukemia, all-trans-retinoic acid (ATRA) increases and activates Casp1 to trigger pyroptosis and differentiation of APL cells [2]. In Alzheimer's disease, strongly enhanced active caspase-1 expression is observed, and Casp1 knockout mice carrying Alzheimer's-associated mutations are protected from spatial memory loss and other sequelae, with reduced brain caspase-1 and interleukin-1β activation [3]. In acute myeloid leukemia, high Casp1 expression is associated with poor prognosis, and its inhibition impairs AML cell proliferation [4].

In conclusion, Casp1 plays a significant role in multiple disease conditions including cancer and neurodegenerative diseases. Gene knockout mouse models have been crucial in revealing its functions in these diseases, such as its involvement in cell death, differentiation, and inflammation, providing insights for potential therapeutic strategies.