In multiple myeloma, colon adenocarcinoma, neuroblastoma, and prostate cancer, overexpression of ID2 stimulates pro-oncogenic activities by inhibiting the pRB tumor suppressor pathway, resulting in cell cycle progression, activation of β-catenin–mediated transcription, and overexpression of the antiapoptotic gene B-cell leukemia-329–32. The gene discussed is ID2; the disease is AL amyloidosis.