MCL pathogenesis and molecular subtypes. MCL primary oncogenic event is the t(11;14) leading to CCND1 overexpression. The differential expression of SOX11 seems to be a relevant factor defining the 2 molecular subtypes. SOX11 expression represses BCL6 that may prevent cells from entering the germinal center. These cells carry unmutated IGHV and are genetically unstable. SOX11 may block the terminal B-cell differentiation of cells by forcing PAX5 expression and promote tumor cell growth, migration, and homing to lymph nodes via activation of the CXCR4/FAK/PI3K/AKT axis. SOX11⁻ MCL cells enter the germinal center, carry mutated IGHV, and are genetically stable. The SOX11⁻ tumor cells have very low invasive potential and remain in the blood as leukemic disease. Both MCL subtypes, conventional and leukemic nonnodal, may acquire additional genetic events such as TP53 mutations than promote progression to aggressive variants.