In a publication in the Journal of Clinical Investigation, Ying et al1 unveil novel immune-mediated mechanisms by which monoclonal immunoglobulin free light chains (FLCs) induce kidney damage, further characterizing the inflammatory pathways activated by the tubular catabolism of these proteins. Endocytosed FLCs were shown previously to induce reactive oxygen species (ROS) generation and intracellular oxidative stress. H2O2 formed by FLCs through direct interaction with water was identified as the molecular event priming the activation of a proinflammatory pathway.