Concerning the role of SND1 in SPT6/hTERT signaling, our results not only demonstrated the oncogenic function of SND1 itself in CRC survival but also uncovered its indispensability in the regulation of hTERT expression and tumor growth mediated by SPT6, as evidenced by the reverse of the upregulation of hTERT expression, cell viability, stem‐like properties, and chemotherapeutic resistance caused by SPT6 overexpression upon SND1 knockdown. Here, SUPT6H is linked to colorectal carcinoma.