Microsoft’s new MDASH AI system found 16 Windows vulnerabilities fixed in this month’s Patch Tuesday, including 2 RCE flaws in IKEv2 and TCP/IP.
A critical vulnerability affecting certain configurations of the Exim open-source mail transfer agent could be exploited by an unauthenticated remote attacker to execute arbitrary code.
Identified as CVE-2026–45185, the security issue impacts some Exim versions before 4.99.3 that use the default GNU Transport Layer Security (GnuTLS) library for secure communication. It is a user-after-free (UAF) flaw triggered during the TLS shutdown while handling BDAT chunked SMTP traffic.
Exim frees a TLS transfer buffer but later continues using stale callback references that can write data into the freed memory region, which can lead to unauthenticated remote code execution (RCE).
A cybersecurity researcher has published proof-of-concept (PoC) exploits for two unpatched Microsoft Windows vulnerabilities named YellowKey and GreenPlasma, which are a BitLocker bypass and a privilege-escalation flaw.
Known as Chaotic Eclipse or Nightmare Eclipse, the researcher describes the BitLocker bypass issue as functioning like a backdoor because the vulnerable component is present only in the Windows Recovery Environment (WinRE), which is used to repair boot-related issues in Windows.
The latest exploits follow the researcher’s previous disclosure of the BlueHammer (CVE-2026–33825) and RedSun (no identifier) local privilege escalation (LPE) as zero-day flaws, both of which began to be exploited in the wild shortly after being publicly disclosed.
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Immunotherapy targeting programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) has transformed the management of several types of cancers, including non-oncogene-addicted non-small cell lung cancer (NSCLC) [1], although its efficacy remains limited by resistance mechanisms and constraints inherent to monoclonal antibodies [1]. To overcome these drawbacks, small-molecule PD-L1 inhibitors have been developed, and we previously contributed by identifying the nanomolar triazine-based ligand Tr-10 [2]. In parallel, combinatorial strategies aimed at improving the efficacy of anti-PD-1/PD-L1 immunotherapy have gained increasing attention. Notably, platinum-based chemotherapy combined with immune checkpoint inhibitors is recommended as a first-line treatment for advanced NSCLC with PD-L1 expression <50% [3]. Here, we investigated a novel combination involving our anti-PD-L1, Tr-10 [2], and a bis(phenyl-pyridine)iridium(III) complex, Ir-2 (Fig. 1A) [4]. Iridium (Ir) complexes, unlike platinum drugs, are chemically inert and induce endoplasmic reticulum (ER) stress and overproduction of reactive oxygen species (ROS) [5,6], both culminating in damage-associated molecular pattern (DAMP) release and immunogenic cell death (ICD). Moreover, their photophysical properties enable PD-L1-targeted bioimaging when coupled with PD-L1 ligands (Fig. S1) [7].