The sustained abnormal activation of SREBP2 provides conditions for NLRP3 inflammasome activation [45], and its induced increase in cholesterol synthesis is lipotoxic, making it an important pathogenic factor for NASH [46] and FASN deficiency‐induced HCC44; on the other hand, after liver cells undergo malignant transformation into liver cancer cells, the autophagy induced by SREBP2 activation performs anti‐apoptotic and pro‐invasive roles in the cells [47]. Here, NLRP3 is linked to liver cancer.