The CDKN2A knocked‐out cells showed merely two unique alterations, namely a 7q deletion (7q‐) resulting in an intragenic loss of MAGI2, a gene reported as altered in many tumor types,30, 31 and a gain in 9p involving half of CNTLN, a gene involved in centriole–centriole cohesion and protein localization,32 forming Subclone B detected in all cells at all passages (Figure 1C). The gene discussed is CNTLN; the disease is neoplasm.