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The outbreak of chilblain‐like lesions (CLL) coincidentally to the COVID‐19 pandemic is a topic of great concern. SARS‐CoV‐2 has been hypothesized as the etiologic agent of CLL, on the basis of the temporal correlation between the “burst” of skin manifestations and the viral pandemic. However, the relationship between CLL and COVID‐19 remains unclear, since authors failed to confirm the SARS‐CoV‐2 infection in these patients using a real‐time reverse transcription polymerase chain reaction (rt‐PCR) test from nasopharyngeal swabs, which seldom resulted positive. Indeed, the most recent articles on the prevalence of the SARS‐CoV‐2 infection in CLL reported a positive swab test in only about a fifth of these patients.

SARS‐CoV‐2 has been hypothesized as the aetiologic agent of CLL, on the basis of the temporal correlation between the “burst” of skin manifestations and the viral pandemic, even though we have scarce evidence of swab‐confirmed infections. Authors have therefore suggested some pathogenetic mechanisms such as a delayed immune‐mediated reaction to the virus in genetically‐predisposed patients1 or an early IFN‐I response in young patients, muting early viral replication but also inducing microangiopathic changes.