Recent studies further indicate that not all PLAID cases are attributable to PLCG2 mutations; some lack abnormal transcripts, implying potential non-genetic mechanisms (e.g., novel autoantibodies), locus heterogeneity, or somatic mutations within hematopoietic or mast-cell lineages that generate cold-sensitive cellular subsets [52]. Here, PLCG2 is linked to familial cold autoinflammatory syndrome 3.