HMGB1 and rheumatoid arthritis: The results of the present study suggest that RA-FLS may use the autophagic pathway in which HMGB1 and Beclin-1 (but not the Akt/mTOR pathway) are involved as a survival mechanism to evade the perturbations of cellular biosynthetic processes by the antimetabolite MTX to sustain cell viability in conditions of metabolic stress.