We developed a CLL-like mouse model, by introducing a kinase-inactive PKCα (PKCα-KR) construct in mouse hematopoietic stem/progenitor cells (HSPCs), which resulted in the development of an aggressive subset of CLL in vitro and in vivo, exhibiting an upregulation of ZAP-70, enhanced proliferation and increased tumour load in the lymphoid organs [11]. Here, PRKCA is linked to neoplasm.