Although ACK1- and BRK- genetic deficiency (Sridaran et al., 2022; Haegebarth et al., 2006) or their pharmacological inhibition does not result in spontaneous lupus development in C57BL/6 mice, we show that ACK1 or BRK inhibitors aggravate IgG glomerular deposition in the kidneys of BALB/cByJ mice treated with pristane to induce a lupus-like disease (Satoh and Reeves, 1994) and increases serum autoantibody levels. Here, TNK2 is linked to systemic lupus erythematosus.