Active transcription of SENCR during EC differentiation may be explained as FLI1 by a positive auto-regulatory loop similarly to the lncRNA HULC, in hepatocellular carcinoma which exists as part of an intricate auto-regulatory network resulting in an increase of its own expression.40 Another explanation of the high levels of SENCR expression in hESC-EC and cultured EC may be due to the stability of the RNA after post-transcriptional modification similar to ZFAS1 lncRNA which is extremely stable and highly expressed in mouse neuroblastoma cells.41 The gene discussed is SENCR; the disease is neuroblastoma.