Combined with increased DNA damage (73) which is accompanied with the initiation of senescence, reduced DICER1 non-canonical activities might drive the accumulation of aged FLS resistant to apoptotic stimuli (7) and exhibiting pro-inflammatory capabilities [through IL-6, an essential component of the senescence-associated secretory phenotype (SASP) (74)], a dangerous cocktail likely driving their aggressive phenotype observed in RA patients. The gene discussed is DICER1; the disease is rheumatoid arthritis.