Therefore, these conflicting roles of NLRP12 [306], including i) the NLRP12-assocciated protective pro-inflammatory function, ii) the NLRP12 mutation-associated diseases triggering function, and iii) the NLRP12 negative regulation role described above might have rendered initial attempts for anti-IL-1 therapy difficult and unsuccessful, and may contribute to explain mechanisms underlying resistance to anti-IL-1 therapy observed in patients with CAPS [310]. This evidence concerns the gene IL1B and cryopyrin-associated periodic syndrome.