HHAT and neoplasm: Actually chromosome 3q26 amplification causes the most prevalent copy number gains and this phenomenon drives coordinated overexpression of SOX2 and PRKCI (a protein kinase Ci that phosphorylates SOX2) in majority of human LSCC, activates PRKCI–SOX2–HHAT signaling axis, and ultimately leads to the establishment of a stem-like, LSCC tumor-initiating cell phenotype (Balsara et al., 1997; Justilien et al., 2014).