Current hypotheses propose that genetic variations found in PG patients, such as mutations in PSTPIP1, MEFV, and NOD2, may be linked to various autoinflammatory conditions.[8] Additionally, abnormal activation of T cells and neutrophils, along with elevated levels of cytokines from the IL-1, IL-36, and IL-17 families, is believed to play a pivotal role in the inflammatory process of PG.[1] In the cohort of 14 patients included in this study, 2 had concurrent IBD and 2 had multiple myeloma. This evidence concerns the gene IL17A and AL amyloidosis.