Latest Windows Terminal Updates from Microsoft: Fixes and Enhanced Mark Mode

Microsoft Unveils New Updates for Windows Terminal

Microsoft has announced two updates for Windows Terminal, catering to both stable channel users and those experimenting with preview versions. The latest releases, while modest in scope, aim to enhance overall performance through crucial bug fixes and quality enhancements.

What’s New in Windows Terminal 1.22.10731.0

Bug Fixes

Eliminated a source of deadlocks occurring during console session transitions.

Improved Japanese translations for the features “Split Tab”and “Rename Tab”.

ConPTY Enhancements

ConPTY now effectively tears down when pipes are closed during startup.

Resolved an issue where ConPTY would freeze on startup due to poorly formatted responses to DA1.

What’s New in Windows Terminal 1.23.10732.0 (Pre-release)

Feature Updates

Users can now navigate between embedded hyperlinks in Mark Mode using Tab and Shift+Tab keys.

Bug Fixes

Corrected hyperlink underlining and mouse reports, which were inaccurately positioned by an entire cell.

Reduced the frequency of terminal crashes when tabs are closed rapidly.

Addressed a recurring deadlock issue during console session handoffs.

The About dialog box now behaves more predictably when opened in multiple windows.

Ensured that closing the first tab frees up its associated resources properly.

Fixed graphical glitches identified in the new icon and color pickers within Appearance settings.

Resolved an issue where tearing off a tab would inadvertently cause its panes to disappear.

Session data will now be properly saved upon closing the last terminal window.

Empty windows will no longer trigger an attempt to save upon closure.

Improved Japanese names for “Split Tab”and “Rename Tab”features.

Debugging processes for Terminal (and Conhost) will generate significantly fewer non-critical errors.

ConPTY Improvements

ConPTY effectively tears down if pipes are closed during initial startup.

Resolved startup hang issues related to malformed responses to DA1.