Therefore, the oncogenic function of LNX2 mediated via the maintenance of NOTCH signaling in colorectal carcinoma might not be dependent upon NUMB protein, and the degradation of NUMB triggered by LNX2 depletion could be a secondary effect exerted by unknown regulators whose expression or activities are fortified or de-repressed at low levels of LNX2 expression. This evidence concerns the gene NUMB and colorectal carcinoma.