A woman once branded "Australia's worst female serial killer" has been pardoned after new evidence suggested she did not kill her four infant children.
Kathleen Folbigg spent 20 years in prison after a jury found she killed Caleb, Patrick, Sarah and Laura over a decade.
But a recent inquiry heard scientists believe they may have died naturally.
The 55-year-old's case has been described as one of Australia's greatest miscarriages of justice.
Ms Folbigg has always maintained her innocence, but was in 2003 jailed for 25 years for the murders of three of her children, and the manslaughter of her first son, Caleb.
Each child died suddenly between 1989 and 1999, aged between 19 days and 19 months, with prosecutors at her trial alleging she had smothered them.
Previous appeals and a separate 2019 inquiry into the case found no grounds for reasonable doubt, and gave greater weight to circumstantial evidence in Ms Folbigg's original trial.
But at the fresh inquiry, headed by retired judge Tom Bathurst, prosecutors accepted that research on gene mutations had changed their understanding of the children's deaths.
New South Wales (NSW) Attorney General Michael Daley on Monday announced that Mr Bathurst had come to the "firm view" there was reasonable doubt that Ms Folbigg was guilty of each offence.
As a result, the NSW governor had signed a full pardon, and ordered Ms Folbigg's immediate release from prison.
"It has been a 20-year-long ordeal for her. If she is not out already, she will be soon... I wish her peace," Mr Daley said, adding his thoughts were also with Craig Folbigg, the children's father.
The unconditional pardon does not quash Ms Folbigg's convictions, Mr Daley added. That would be a decision for the Court of Criminal Appeal, if Mr Bathurst chooses to refer the case to it.
The pardon comes after a years-long campaign to free Ms Folbigg, sparked when a team of immunologists found her daughters shared a genetic mutation that can cause sudden cardiac death.
Evidence was also uncovered that Ms Folbigg's sons possessed a different genetic mutation, linked to sudden-onset epilepsy in mice.
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