Increased CAMKII has been observed in liver cancer,[10b] colon cancer,[41] breast cancer,[42] lung cancer,[43] and hematopoietic cancers.[10, 14, 44] In general, the mechanisms by which CAMKII promotes cancers from previous studies are limited to the regulation of signaling pathways directly related to tumor growth such as c‐Myc, JAK/STAT, and AKT pathways. Here, SOAT1 is linked to hematopoietic and lymphoid cell neoplasm.