Our study revealed that during NASH-to-HCC progression, dysregulation of the α1-NKA signalosome upregulates survivin with concomitant downregulation of SMAC expression through the PI3K → Akt → S6K1 signaling pathway, favoring a change from programmed cell death to uncontrolled division. This evidence concerns the gene BIRC5 and metabolic dysfunction-associated steatohepatitis.