Mice with germline deletion (Famin–/–) or engineered to express human non-risk, risk, and monogenic disease FAMIN variants (Faminp.254I, Faminp.254V, and Faminp.284R, respectively) revealed that reduced or absent FAMIN activity increases the severity of experimental sepsis and arthritis (Cader et al., 2016, Skon-Hegg et al., 2019). This evidence concerns the gene LACC1 and arthritic joint disease.