This month’s issue of Going on Trial takes a sneak peek at some early null results from a small trial of a cannabidiol-based drug for autism, among other recent drug developments.

Autistic children taking the drug showed improvements in some behaviors but not in their social skills.

People whose brains look like those of people who carry autism-linked copy number variants also share markers of heart health.

Many autism-linked genes are somehow tied to cilia, the tiny hair-like sensors that stud a cell’s surface. But the question remains whether, and how, cilia differences contribute to the condition.

Faulty mTOR signaling, implicated in syndromic forms of autism, also hinders cells grown from people with idiopathic autism or autism-linked deletions on chromosome 16.

Within the 16p region of the genome, the two types of variants similarly decrease neuronal gene expression — an effect that may reflect their spatial relationship.

The signal, called CD47, is disrupted in autistic people who have a larger-than-average head.

Restoring the gene, TAOK2, in mice missing an autism-linked region of chromosome 16 normalizes neuronal movement during development.

The results highlight the importance of subgrouping study participants based on their underlying genetics, the researchers say.

The method, called Orgo-Seq, reveals that a deletion of genes on chromosome 16 increases the proportion of immature neurons and neural precursors in brain organoids derived from people with the mutation.