BAP1-ASXL2, but not ASXL1-BAP1 complexes, appears to mediate this tumor-suppressive function; overexpression of BAP1 or ASXL2, but not ASXL1, induces senescence, and deletion of the ASXM domain of ASXL2 impairs senescence (human fibroblasts IMR90 cell line) [99]. The gene discussed is BAP1; the disease is neoplasm.